Skip to main content

Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles and JavaScript.

  • Review Article
  • Published:

Differential roles of eosinophils in cardiovascular disease

Nature Reviews Cardiology (2024)Cite this article

Subjects

Abstract

Eosinophils are essential innate immune cells in allergic responses. Accumulating evidence indicates that eosinophils also participate in the pathogenesis of cardiovascular diseases (CVDs). In clinical studies, high blood eosinophil counts and eosinophil cationic protein levels have been associated with an increased risk of CVD, including myocardial infarction (MI), cardiac hypertrophy, atrial fibrillation, abdominal aortic aneurysm (AAA) and atherosclerosis. However, low blood eosinophil counts have also been reported to be a risk factor for MI, heart failure, aortic dissection, AAA, deep vein thrombosis, pulmonary embolism and ischaemic stroke. Although these conflicting clinical observations remain unexplained, CVD status, timing of eosinophil data collection, and tissue eosinophil phenotypic and functional heterogeneities might account for these discrepancies. Preclinical studies suggest that eosinophils have protective actions in MI, cardiac hypertrophy, heart failure and AAA. By contrast, cationic proteins and platelet-activating factor from eosinophils have been shown to promote vascular smooth muscle cell proliferation, vascular calcification, thrombomodulin inactivation and platelet activation and aggregation, thereby exacerbating atherosclerosis, atrial fibrillation, thrombosis and associated complications. Therefore, eosinophils seem to promote calcification and thrombosis in chronic CVD but are protective in acute cardiovascular settings. In this Review, we summarize the available clinical and preclinical data on the different roles of eosinophils in CVD.

Key points

  • High blood eosinophil counts and eosinophil cationic protein levels have been suggested to predict a higher risk of cardiovascular disease in humans; however, other studies suggest that low blood eosinophil counts are also predictive of increased risk of cardiovascular disease.

  • Disease status and timing of collection of blood eosinophil data can influence risk assessment, with low blood eosinophil counts being a risk factor for acute cardiovascular events or being detected from early data collection after the events.

  • Low eosinophil counts and high cationic protein levels are associated with a higher risk of thrombosis, ischaemic stroke, deep vein thrombosis and pulmonary embolism.

  • In preclinical models of myocardial infarction, cardiac hypertrophy or heart failure, eosinophil cationic proteins, IL-4 and IL-13 limit cardiomyocyte death and hypertrophy, inhibit cardiac fibrosis and promote M2-like macrophage polarization.

  • Eosinophils might protect against aortic dissection and abdominal aortic aneurysms by controlling angiogenesis, monocyte and macrophage polarization, and aortic vascular and immune cell activation.

  • Eosinophils promote atherogenesis through the production of cationic proteins and platelet-activating factor to stimulate platelets and thrombosis, recruit platelets to the endothelium and induce vascular calcification.

This is a preview of subscription content, access via your institution

Access options

Buy this article

  • Purchase on SpringerLink
  • Instant access to full article PDF
Buy now

Prices may be subject to local taxes which are calculated during checkout

Fig. 1: Eosinophils in atherosclerosis.
Fig. 2: Eosinophils and ILC2s in myocardial infarction.
Fig. 3: Eosinophils in cardiac hypertrophy and heart failure.
Fig. 4: Eosinophil functions in thrombosis.
Fig. 5: Eosinophils and ILC2s in aortic abdominal aneurysm.

Similar content being viewed by others

References

  1. Khoury, P., Grayson, P. C. & Klion, A. D. Eosinophils in vasculitis: characteristics and roles in pathogenesis. Nat. Rev. Rheumatol. 10, 474–483 (2014).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  2. Wen, T. & Rothenberg, M. E. The regulatory function of eosinophils. Microbiol. Spectr. https://doi.org/10.1128/microbiolspec.MCHD-0020-2015 (2016).

  3. Takatsu, K. Interleukin-5 and IL-5 receptor in health and diseases. Proc. Jpn Acad. Ser. B Phys. Biol. Sci. 87, 463–485 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  4. Takatsu, K. & Nakajima, H. IL-5 and eosinophilia. Curr. Opin. Immunol. 20, 288–294 (2008).

    Article  CAS  PubMed  Google Scholar 

  5. Kouro, T. & Takatsu, K. IL-5- and eosinophil-mediated inflammation: from discovery to therapy. Int. Immunol. 21, 1303–1309 (2009).

    Article  CAS  PubMed  Google Scholar 

  6. Ramirez, G. A. et al. Eosinophils from physiology to disease: a comprehensive review. Biomed. Res. Int. 2018, 9095275 (2018).

    Article  PubMed  PubMed Central  Google Scholar 

  7. Wu, D. et al. Eosinophils sustain adipose alternatively activated macrophages associated with glucose homeostasis. Science 332, 243–247 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  8. Molofsky, A. B. et al. Innate lymphoid type 2 cells sustain visceral adipose tissue eosinophils and alternatively activated macrophages. J. Exp. Med. 210, 535–549 (2013).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  9. Lee, E. H. et al. Eosinophils support adipocyte maturation and promote glucose tolerance in obesity. Sci. Rep. 8, 9894 (2018).

    Article  PubMed  PubMed Central  Google Scholar 

  10. Davoine, F. & Lacy, P. Eosinophil cytokines, chemokines, and growth factors: emerging roles in immunity. Front. Immunol. 5, 570 (2014).

    Article  PubMed  PubMed Central  Google Scholar 

  11. Hams, E., Locksley, R. M., McKenzie, A. N. & Fallon, P. G. Cutting edge: IL-25 elicits innate lymphoid type 2 and type II NKT cells that regulate obesity in mice. J. Immunol. 191, 5349–5353 (2013).

    Article  CAS  PubMed  Google Scholar 

  12. Mesnil, C. et al. Lung-resident eosinophils represent a distinct regulatory eosinophil subset. J. Clin. Invest. 126, 3279–3295 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  13. Bousquet, J. et al. Eosinophilic inflammation in asthma. N. Engl. J. Med. 323, 1033–1039 (1990).

    Article  CAS  PubMed  Google Scholar 

  14. McBrien, C. N. & Menzies-Gow, A. The biology of eosinophils and their role in asthma. Front. Med. 4, 93 (2017).

    Article  Google Scholar 

  15. Hartl, S. et al. Blood eosinophil count in the general population: typical values and potential confounders. Eur. Respir. J. 55, 1901874 (2020).

    Article  CAS  PubMed  Google Scholar 

  16. Liu, C. L. et al. Allergic lung inflammation aggravates angiotensin II-induced abdominal aortic aneurysms in mice. Arterioscler. Thromb. Vasc. Biol. 36, 69–77 (2016).

    Article  PubMed  Google Scholar 

  17. Liu, C. L. et al. Allergic lung inflammation promotes atherosclerosis in apolipoprotein E-deficient mice. Transl. Res. 171, 1–16 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  18. Liu, C. L. et al. Asthma associates with human abdominal aortic aneurysm and rupture. Arterioscler. Thromb. Vasc. Biol. 36, 570–578 (2016).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  19. Guo, J. et al. Allergic asthma is a risk factor for human cardiovascular diseases. Nat. Cardiovasc. Res. 1, 417–430 (2022).

    Article  PubMed  Google Scholar 

  20. Liu, C. L. et al. Eosinophils protect mice from angiotensin-II perfusion-induced abdominal aortic aneurysm. Circ. Res. 128, 188–202 (2021).

    Article  CAS  PubMed  Google Scholar 

  21. Meng, Z. et al. Cationic proteins from eosinophils bind bone morphogenetic protein receptors promoting vascular calcification and atherogenesis. Eur. Heart J. 44, 2763–2783 (2023).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  22. Welsh, C. et al. Association of total and differential leukocyte counts with cardiovascular disease and mortality in the UK Biobank. Arterioscler. Thromb. Vasc. Biol. 38, 1415–1423 (2018).

    Article  CAS  PubMed  Google Scholar 

  23. Groot, H. E., van Blokland, I. V., Lipsic, E., Karper, J. C. & van der Harst, P. Leukocyte profiles across the cardiovascular disease continuum: a population-based cohort study. J. Mol. Cell. Cardiol. 138, 158–164 (2020).

    Article  CAS  PubMed  Google Scholar 

  24. Nadimi, A. E., Ahmadi, J. & Mehrabian, M. Peripheral eosinophil count and allergy in patients with coronary artery disease. Acta Med. Indones. 40, 74–77 (2008).

    PubMed  Google Scholar 

  25. Pongdee, T. et al. Rethinking blood eosinophil counts: epidemiology, associated chronic diseases, and increased risks of cardiovascular disease. J. Allergy Clin. Immunol. Glob. 1, 233–240 (2022).

    Article  PubMed  PubMed Central  Google Scholar 

  26. Niccoli, G. et al. Pre-intervention eosinophil cationic protein serum levels predict clinical outcomes following implantation of drug-eluting stents. Eur. Heart J. 30, 1340–1347 (2009).

    Article  CAS  PubMed  Google Scholar 

  27. Quinta, J. B. et al. Cardiovascular adverse effects of anti-IL-5/IL-5Ralpha therapies: a real-world study. J. Allergy Clin. Immunol. Pract. 9, 1411–1413 (2021).

    Article  CAS  PubMed  Google Scholar 

  28. Verdoia, M. et al. Absolute eosinophils count and the extent of coronary artery disease: a single centre cohort study. J. Thromb. Thrombolysis 39, 459–466 (2015).

    Article  PubMed  Google Scholar 

  29. Shah, A. D., Denaxas, S., Nicholas, O., Hingorani, A. D. & Hemingway, H. Low eosinophil and low lymphocyte counts and the incidence of 12 cardiovascular diseases: a CALIBER cohort study. Open Heart 3, e000477 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  30. Gao, S. et al. Eosinophils count in peripheral circulation is associated with coronary artery disease. Atherosclerosis 286, 128–134 (2019).

    Article  CAS  PubMed  Google Scholar 

  31. Liu, T. et al. Group 2 innate lymphoid cells protect mouse heart from myocardial infarction injury via interleukin 5, eosinophils, and dendritic cells. Cardiovasc. Res. 119, 1046–1061 (2023).

    Article  CAS  PubMed  Google Scholar 

  32. Zhang, Y. et al. Group 2 innate lymphoid cells protect mice from abdominal aortic aneurysm formation via IL5 and eosinophils. Adv. Sci. 10, e2206958 (2023).

    Article  Google Scholar 

  33. Yang, C. et al. Eosinophils protect pressure overload- and beta-adrenoreceptor agonist-induced cardiac hypertrophy. Cardiovasc. Res. 119, 195–212 (2023).

    Article  CAS  PubMed  Google Scholar 

  34. Liu, J. et al. Eosinophils improve cardiac function after myocardial infarction. Nat. Commun. 11, 6396 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  35. Xu, J. Y. et al. Interleukin-5-induced eosinophil population improves cardiac function after myocardial infarction. Cardiovasc. Res. 118, 2165–2178 (2022).

    Article  CAS  PubMed  Google Scholar 

  36. Yu, X. et al. Innate lymphoid cells promote recovery of ventricular function after myocardial infarction. J. Am. Coll. Cardiol. 78, 1127–1142 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  37. Knutsson, A. et al. Associations of interleukin-5 with plaque development and cardiovascular events. JACC Basic Transl. Sci. 4, 891–902 (2019).

    Article  PubMed  PubMed Central  Google Scholar 

  38. Gu, L. et al. The relationship between interleukin-4 levels and cardiovascular events in patients with chronic kidney disease. Risk Manag. Healthc. Policy 13, 2371–2377 (2020).

    Article  PubMed  PubMed Central  Google Scholar 

  39. Silveira, A. et al. Plasma IL-5 concentration and subclinical carotid atherosclerosis. Atherosclerosis 239, 125–130 (2015).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  40. Venge, P. et al. Eosinophil cationic protein (ECP): molecular and biological properties and the use of ECP as a marker of eosinophil activation in disease. Clin. Exp. Allergy 29, 1172–1186 (1999).

    Article  CAS  PubMed  Google Scholar 

  41. Lehrer, R. I. et al. Antibacterial properties of eosinophil major basic protein and eosinophil cationic protein. J. Immunol. 142, 4428–4434 (1989).

    Article  CAS  PubMed  Google Scholar 

  42. Chihara, J. et al. Possible release of eosinophil granule proteins in response to signaling from intercellular adhesion molecule-1 and its ligands. Int. Arch. Allergy Immunol. 108, 52–54 (1995).

    Article  CAS  PubMed  Google Scholar 

  43. Hernnas, J. et al. Eosinophil cationic protein alters proteoglycan metabolism in human lung fibroblast cultures. Eur. J. Cell Biol. 59, 352–363 (1992).

    CAS  PubMed  Google Scholar 

  44. Pickett, J. R., Wu, Y., Zacchi, L. F. & Ta, H. T. Targeting endothelial vascular cell adhesion molecule-1 in atherosclerosis: drug discovery and development of vascular cell adhesion molecule-1-directed novel therapeutics. Cardiovasc. Res. 119, 2278–2293 (2023).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  45. Barallobre-Barreiro, J. et al. Extracellular matrix in heart failure: role of ADAMTS5 in proteoglycan remodeling. Circulation 144, 2021–2034 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  46. Halim, T. Y. et al. Group 2 innate lymphoid cells are critical for the initiation of adaptive T helper 2 cell-mediated allergic lung inflammation. Immunity 40, 425–435 (2014).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  47. Kamijo, S. et al. IL-33-mediated innate response and adaptive immune cells contribute to maximum responses of protease allergen-induced allergic airway inflammation. J. Immunol. 190, 4489–4499 (2013).

    Article  CAS  PubMed  Google Scholar 

  48. Doherty, T. A. At the bench: understanding group 2 innate lymphoid cells in disease. J. Leukoc. Biol. 97, 455–467 (2015).

    Article  CAS  PubMed  Google Scholar 

  49. Pelaia, C. et al. Interleukin-5 in the pathophysiology of severe asthma. Front. Physiol. 10, 1514 (2019).

    Article  PubMed  PubMed Central  Google Scholar 

  50. Kitano, T. et al. Association between absolute eosinophil count and complex aortic arch plaque in patients with acute ischemic stroke. Stroke 48, 1074–1076 (2017).

    Article  PubMed  Google Scholar 

  51. Xu, W. J. et al. Arterial and venous thromboembolism risk associated with blood eosinophils: a systematic review and meta-analysis. Anim. Model Exp. Med. 5, 470–481 (2022).

    Article  CAS  Google Scholar 

  52. Spriewald, B. M., Ensminger, S. M., Billing, J. S., Morris, P. J. & Wood, K. J. Increased expression of transforming growth factor-beta and eosinophil infiltration is associated with the development of transplant arteriosclerosis in long-term surviving cardiac allografts. Transplantation 76, 1105–1111 (2003).

    Article  CAS  PubMed  Google Scholar 

  53. Marx, C. et al. Eosinophil–platelet interactions promote atherosclerosis and stabilize thrombosis with eosinophil extracellular traps. Blood 134, 1859–1872 (2019).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  54. Brinkmann, V. et al. Neutrophil extracellular traps kill bacteria. Science 303, 1532–1535 (2004).

    Article  CAS  PubMed  Google Scholar 

  55. Doring, Y., Libby, P. & Soehnlein, O. Neutrophil extracellular traps participate in cardiovascular diseases: recent experimental and clinical insights. Circ. Res. 126, 1228–1241 (2020).

    Article  PubMed  PubMed Central  Google Scholar 

  56. Thakur, M. et al. NETs-induced thrombosis impacts on cardiovascular and chronic kidney disease. Circ. Res. 132, 933–949 (2023).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  57. Riascos-Bernal, D. F. & Sibinga, N. E. Neutrophil extracellular traps in cardiac hypertrophy: a KLF2 perspective. J. Clin. Invest. 132, e156453 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  58. Yousefi, S. et al. Catapult-like release of mitochondrial DNA by eosinophils contributes to antibacterial defense. Nat. Med. 14, 949–953 (2008).

    Article  CAS  PubMed  Google Scholar 

  59. Mukai, H. Y., Ninomiya, H., Ohtani, K., Nagasawa, T. & Abe, T. Major basic protein binding to thrombomodulin potentially contributes to the thrombosis in patients with eosinophilia. Br. J. Haematol. 90, 892–899 (1995).

    Article  CAS  PubMed  Google Scholar 

  60. Slungaard, A., Vercellotti, G. M., Tran, T., Gleich, G. J. & Key, N. S. Eosinophil cationic granule proteins impair thrombomodulin function. A potential mechanism for thromboembolism in hypereosinophilic heart disease. J. Clin. Invest. 91, 1721–1730 (1993).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  61. Mukherjee, M., Lacy, P. & Ueki, S. Eosinophil extracellular traps and inflammatory pathologies — untangling the web! Front. Immunol. 9, 2763 (2018).

    Article  PubMed  PubMed Central  Google Scholar 

  62. Ueki, S. et al. Eosinophil ETosis and DNA traps: a new look at eosinophilic inflammation. Curr. Allergy Asthma Rep. 16, 54 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  63. Choi, Y. et al. Eosinophil extracellular traps activate type 2 innate lymphoid cells through stimulating airway epithelium in severe asthma. Allergy 75, 95–103 (2020).

    Article  CAS  PubMed  Google Scholar 

  64. Olsson, I. & Venge, P. Cationic proteins of human granulocytes. I. Isolation of the cationic proteins from the granules of leukaemic myeloid cells. Scand. J. Haematol. 9, 204–214 (1972).

    Article  CAS  PubMed  Google Scholar 

  65. Gleich, G. J., Loegering, D. A. & Maldonado, J. E. Identification of a major basic protein in guinea pig eosinophil granules. J. Exp. Med. 137, 1459–1471 (1973).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  66. Venge, P., Zetterstrom, O., Dahl, R., Roxin, L. E. & Olsson, I. Low levels of eosinophil cationic proteins in patients with asthma. Lancet 2, 373–375 (1977).

    Article  CAS  PubMed  Google Scholar 

  67. Hallgren, R., Venge, P., Cullhed, I. & Olsson, I. Blood eosinophils and eosinophil cationic protein after acute myocardial infarction or corticosteroid administration. Br. J. Haematol. 42, 147–154 (1979).

    Article  CAS  PubMed  Google Scholar 

  68. Margolis, J. R. et al. The diagnostic and prognostic significance of coronary artery calcification. A report of 800 cases. Radiology 137, 609–616 (1980).

    Article  CAS  PubMed  Google Scholar 

  69. Baumgart, D. et al. Comparison of electron beam computed tomography with intracoronary ultrasound and coronary angiography for detection of coronary atherosclerosis. J. Am. Coll. Cardiol. 30, 57–64 (1997).

    Article  CAS  PubMed  Google Scholar 

  70. Mintz, G. S. et al. Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study. J. Am. Coll. Cardiol. 29, 268–274 (1997).

    Article  CAS  PubMed  Google Scholar 

  71. Tanaka, M. et al. Eosinophil count is positively correlated with coronary artery calcification. Hypertens. Res. 35, 325–328 (2012).

    Article  PubMed  Google Scholar 

  72. Hou, L. et al. White blood cell count in young adulthood and coronary artery calcification in early middle age: Coronary Artery Risk Development in Young Adults (CARDIA) study. Eur. J. Epidemiol. 28, 735–742 (2013).

    Article  PubMed  PubMed Central  Google Scholar 

  73. Diederichsen, A. C. et al. The Danish Cardiovascular Screening Trial (DANCAVAS): study protocol for a randomized controlled trial. Trials 16, 554 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  74. Toor, I. S. et al. Eosinophil deficiency promotes aberrant repair and adverse remodeling following acute myocardial infarction. JACC Basic Transl. Sci. 5, 665–681 (2020).

    Article  PubMed  PubMed Central  Google Scholar 

  75. Qin, M. et al. Oxidized LDL activated eosinophil polarize macrophage phenotype from M2 to M1 through activation of CD36 scavenger receptor. Atherosclerosis 263, 82–91 (2017).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  76. Sawada, N. et al. Circulating oxidized LDL, increased in patients with acute myocardial infarction, is accompanied by heavily modified HDL. J. Lipid Res. 61, 816–829 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  77. Nordin Fredrikson, G., Hedblad, B., Berglund, G. & Nilsson, J. Plasma oxidized LDL: a predictor for acute myocardial infarction? J. Intern. Med. 253, 425–429 (2003).

    Article  CAS  PubMed  Google Scholar 

  78. Deng, Y. et al. Unique phenotypes of heart resident type 2 innate lymphoid cells. Front. Immunol. 11, 802 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  79. Yu, H., Wei, Y., Dong, Y. & Chen, P. Regulation of notch signaling pathway to innate lymphoid cells in patients with acute myocardial infarction. Immunol. Invest. 52, 241–255 (2023).

    Article  CAS  PubMed  Google Scholar 

  80. Niccoli, G. et al. Eosinophil cationic protein: a new biomarker of coronary atherosclerosis. Atherosclerosis 211, 606–611 (2010).

    Article  CAS  PubMed  Google Scholar 

  81. Niccoli, G. et al. Allergic inflammation is associated with coronary instability and a worse clinical outcome after acute myocardial infarction. Circ. Cardiovasc. Interv. 8, e002554 (2015).

    Article  CAS  PubMed  Google Scholar 

  82. Xia, G. L., Wang, Y. K. & Huang, Z. Q. The correlation of serum myeloid-related protein-8/14 and eosinophil cationic protein in patients with coronary artery disease. Biomed. Res. Int. 2016, 4980251 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  83. Guner, A. et al. Eosinophil percentage as a new prognostic marker in patients with ST-segment elevation myocardial infarction undergoing primary percutaneous coronary intervention. Interv. Med. Appl. Sci. 11, 146–153 (2020).

    PubMed  Google Scholar 

  84. Jiang, P., Wang, D. Z., Ren, Y. L., Cai, J. P. & Chen, B. X. Significance of eosinophil accumulation in the thrombus and decrease in peripheral blood in patients with acute coronary syndrome. Coron. Artery Dis. 26, 101–106 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  85. Sincer, I., Gunes, Y., Mansiroglu, A. K. & Aktas, G. Differential value of eosinophil count in acute coronary syndrome among elderly patients. Aging Male 23, 958–961 (2020).

    Article  PubMed  Google Scholar 

  86. Sasmita, B. R. et al. Leukocyte and its subtypes as predictors of short-term outcome in cardiogenic shock complicating acute myocardial infarction: a cohort study. Shock 57, 351–359 (2022).

    Article  PubMed  Google Scholar 

  87. Ye, L. et al. Combination of eosinophil percentage and high-sensitivity C-reactive protein predicts in-hospital major adverse cardiac events in ST-elevation myocardial infarction patients undergoing primary percutaneous coronary intervention. J. Clin. Lab. Anal. 34, e23367 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  88. Alkhalil, M. et al. Eosinopenia as an adverse marker of clinical outcomes in patients presenting with acute myocardial infarction. Am. J. Med. 132, e827–e834 (2019).

    Article  PubMed  Google Scholar 

  89. Niccoli, G., Kharbanda, R. K., Crea, F. & Banning, A. P. No-reflow: again prevention is better than treatment. Eur. Heart J. 31, 2449–2455 (2010).

    Article  PubMed  Google Scholar 

  90. Rezkalla, S. H., Stankowski, R. V., Hanna, J. & Kloner, R. A. Management of no-reflow phenomenon in the catheterization laboratory. JACC Cardiovasc. Interv. 10, 215–223 (2017).

    Article  PubMed  Google Scholar 

  91. Mo, D. G., Wang, C. S., Liu, J. H. & Li, T. The predictive value of eosinophil levels on no-reflow in patients with STEMI following PCI: a retrospective cohort study. Sci. Rep. 12, 17862 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  92. Toor, I. S., Jaumdally, R., Lip, G. Y., Millane, T. & Varma, C. Eosinophil count predicts mortality following percutaneous coronary intervention. Thromb. Res. 130, 607–611 (2012).

    Article  CAS  PubMed  Google Scholar 

  93. Rios-Navarro, C. et al. Characterization and implications of the dynamics of eosinophils in blood and in the infarcted myocardium after coronary reperfusion. PLoS ONE 13, e0206344 (2018).

    Article  PubMed  PubMed Central  Google Scholar 

  94. Caforio, A. L. et al. Current state of knowledge on aetiology, diagnosis, management, and therapy of myocarditis: a position statement of the European Society of Cardiology Working Group on Myocardial and Pericardial Diseases. Eur. Heart J. 34, 2636–2648 (2013).

    Article  PubMed  Google Scholar 

  95. Oakley, C. M. & Olsen, G. J. Eosinophilia and heart disease. Br. Heart J. 39, 233–237 (1977).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  96. Cugno, M., Marzano, A. V., Lorini, M., Carbonelli, V. & Tedeschi, A. Enhanced tissue factor expression by blood eosinophils from patients with hypereosinophilia: a possible link with thrombosis. PLoS ONE 9, e111862 (2014).

    Article  PubMed  PubMed Central  Google Scholar 

  97. Seguela, P. E. et al. Eosinophilic cardiac disease: molecular, clinical and imaging aspects. Arch. Cardiovasc. Dis. 108, 258–268 (2015).

    Article  PubMed  Google Scholar 

  98. Akuthota, P. & Weller, P. F. Spectrum of eosinophilic end-organ manifestations. Immunol. Allergy Clin. North. Am. 35, 403–411 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  99. Diny, N. L. et al. Macrophages and cardiac fibroblasts are the main producers of eotaxins and regulate eosinophil trafficking to the heart. Eur. J. Immunol. 46, 2749–2760 (2016).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  100. Brambatti, M. et al. Eosinophilic myocarditis: characteristics, treatment, and outcomes. J. Am. Coll. Cardiol. 70, 2363–2375 (2017).

    Article  PubMed  Google Scholar 

  101. Corradi, D. et al. Eosinophilic myocarditis in a patient with idiopathic hypereosinophilic syndrome: insights into mechanisms of myocardial cell death. Hum. Pathol. 35, 1160–1163 (2004).

    Article  PubMed  Google Scholar 

  102. Janin, A. Eosinophilic myocarditis and fibrosis. Hum. Pathol. 36, 592–593 (2005).

    Article  PubMed  Google Scholar 

  103. Hirasawa, M., Deguchi, H., Ukimura, A. & Kitaura, Y. Immunologic interaction between infiltrating eosinophils and T lymphocytes in murine spontaneous eosinophilic myocarditis. Int. Arch. Allergy Immunol. 130, 73–81 (2003).

    Article  CAS  PubMed  Google Scholar 

  104. Prows, D. R., Klingler, A., Gibbons, W. J. Jr, Homan, S. M. & Zimmermann, N. Characterization of a mouse model of hypereosinophilia-associated heart disease. Am. J. Physiol. Heart Circ. Physiol. 317, H405–H414 (2019).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  105. Ogbogu, P. U., Rosing, D. R. & Horne, M. K. III Cardiovascular manifestations of hypereosinophilic syndromes. Immunol. Allergy Clin. North. Am. 27, 457–475 (2007).

    Article  PubMed  PubMed Central  Google Scholar 

  106. Ong, S. et al. Natural killer cells limit cardiac inflammation and fibrosis by halting eosinophil infiltration. Am. J. Pathol. 185, 847–861 (2015).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  107. Barin, J. G. et al. Fatal eosinophilic myocarditis develops in the absence of IFN-gamma and IL-17A. J. Immunol. 191, 4038–4047 (2013).

    Article  CAS  PubMed  Google Scholar 

  108. Diny, N. L. et al. Eosinophil-derived IL-4 drives progression of myocarditis to inflammatory dilated cardiomyopathy. J. Exp. Med. 214, 943–957 (2017).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  109. Zanchetti, A. Hypertension: cardiac hypertrophy as a target of antihypertensive therapy. Nat. Rev. Cardiol. 7, 66–67 (2010).

    Article  CAS  PubMed  Google Scholar 

  110. Rader, F., Sachdev, E., Arsanjani, R. & Siegel, R. J. Left ventricular hypertrophy in valvular aortic stenosis: mechanisms and clinical implications. Am. J. Med. 128, 344–352 (2015).

    Article  PubMed  Google Scholar 

  111. Tardiff, J. C. Cardiac hypertrophy: stressing out the heart. J. Clin. Invest. 116, 1467–1470 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  112. Shimizu, I. & Minamino, T. Physiological and pathological cardiac hypertrophy. J. Mol. Cell Cardiol. 97, 245–262 (2016).

    Article  CAS  PubMed  Google Scholar 

  113. Vural, A. & Aydin, E. The predictive value of eosinophil indices for major cardiovascular events in patients with acute decompensated HFrEF. Medicina 58, 1455 (2022).

    Article  PubMed  PubMed Central  Google Scholar 

  114. Silva, N., Patricio, E., Bettencourt, P. & Guimaraes, J. T. Evaluation of innate immunity biomarkers on admission and at discharge from an acute heart failure episode. J. Clin. Lab. Anal. 30, 1183–1190 (2016).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  115. Dembic, M., Hedley, P. L., Torp-Pedersen, C., Kober, L. & Christiansen, M. Pregnancy-associated plasma protein-A (PAPP-A) and the proform of the eosinophil major basic protein (ProMBP) are associated with increased risk of death in heart failure patients. Scand. J. Clin. Lab. Invest. 77, 352–357 (2017).

    Article  CAS  PubMed  Google Scholar 

  116. Go, A. S. et al. Prevalence of diagnosed atrial fibrillation in adults: national implications for rhythm management and stroke prevention: the Anticoagulation and Risk Factors in Atrial Fibrillation (ATRIA) study. JAMA 285, 2370–2375 (2001).

    Article  CAS  PubMed  Google Scholar 

  117. European Heart Rhythm Association et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation — executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients With Atrial Fibrillation). J. Am. Coll. Cardiol. 48, 854–906 (2006).

    Article  Google Scholar 

  118. Falk, R. H. Atrial fibrillation. N. Engl. J. Med. 344, 1067–1078 (2001).

    Article  CAS  PubMed  Google Scholar 

  119. Lip, G. Y. Does atrial fibrillation confer a hypercoagulable state? Lancet 346, 1313–1314 (1995).

    Article  CAS  PubMed  Google Scholar 

  120. Misialek, J. R. et al. Association of white blood cell count and differential with the incidence of atrial fibrillation: the Atherosclerosis Risk in Communities (ARIC) study. PLoS ONE 10, e0136219 (2015).

    Article  PubMed  PubMed Central  Google Scholar 

  121. Chen, P., Chen, J., Xie, X., Zhu, J. & Xia, L. Eosinophils in patients with lone atrial fibrillation. Pacing Clin. Electrophysiol. 40, 955–958 (2017).

    Article  PubMed  Google Scholar 

  122. Kecoglu, S., Demir, M., Uyan, U. & Melek, M. The effects of eosinophil on the left atrial thrombus in patients with atrial fibrillation. Clin. Appl. Thromb. Hemost. 20, 285–289 (2014).

    Article  PubMed  Google Scholar 

  123. Cavallari, I. & Patti, G. Early risk of mortality, cardiovascular events, and bleeding in patients with newly diagnosed atrial fibrillation. Eur. Heart J. Suppl. 22, L110–L113 (2020).

    Article  PubMed  PubMed Central  Google Scholar 

  124. Owens, A. P. III & Mackman, N. Tissue factor and thrombosis: the clot starts here. Thromb. Haemost. 104, 432–439 (2010).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  125. Leiva, O. et al. Association of thrombosis with hypereosinophilic syndrome in patients with genetic alterations. JAMA Netw. Open 4, e2119812 (2021).

    Article  PubMed  PubMed Central  Google Scholar 

  126. Fujita, K., Ishimaru, H., Hatta, K. & Kobashi, Y. Hypereosinophilic syndrome as a cause of fatal thrombosis: two case reports with histological study. J. Thromb. Thrombolysis 40, 255–259 (2015).

    Article  PubMed  Google Scholar 

  127. Slungaard, A. & Mahoney, J. R. Jr. Thiocyanate is the major substrate for eosinophil peroxidase in physiologic fluids. Implications for cytotoxicity. J. Biol. Chem. 266, 4903–4910 (1991).

    Article  CAS  PubMed  Google Scholar 

  128. Wang, J. G. et al. The principal eosinophil peroxidase product, HOSCN, is a uniquely potent phagocyte oxidant inducer of endothelial cell tissue factor activity: a potential mechanism for thrombosis in eosinophilic inflammatory states. Blood 107, 558–565 (2006).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  129. Maruyama, I., Bell, C. E. & Majerus, P. W. Thrombomodulin is found on endothelium of arteries, veins, capillaries, and lymphatics, and on syncytiotrophoblast of human placenta. J. Cell Biol. 101, 363–371 (1985).

    Article  CAS  PubMed  Google Scholar 

  130. Dittman, W. A. & Majerus, P. W. Structure and function of thrombomodulin: a natural anticoagulant. Blood 75, 329–336 (1990).

    Article  CAS  PubMed  Google Scholar 

  131. Esmon, C. T. The roles of protein C and thrombomodulin in the regulation of blood coagulation. J. Biol. Chem. 264, 4743–4746 (1989).

    Article  CAS  PubMed  Google Scholar 

  132. Esmon, C. T. Molecular events that control the protein C anticoagulant pathway. Thromb. Haemost. 70, 29–35 (1993).

    Article  CAS  PubMed  Google Scholar 

  133. Takano, S. Role of 5-hydroxytryptamine in platelet thrombus formation and mechanisms of inhibition of thrombus formation by 5-hydroxytryptamine2A antagonists in rabbits. Arch. Int. Pharmacodyn. Ther. 330, 297–308 (1995).

    CAS  PubMed  Google Scholar 

  134. Rohrbach, M. S., Wheatley, C. L., Slifman, N. R. & Gleich, G. J. Activation of platelets by eosinophil granule proteins. J. Exp. Med. 172, 1271–1274 (1990).

    Article  CAS  PubMed  Google Scholar 

  135. Cargill, D. I., Cohen, D. S., Van Valen, R. G., Klimek, J. J. & Levin, R. P. Aggregation, release and desensitization induced in platelets from five species by platelet activating factor (PAF). Thromb. Haemost. 49, 204–207 (1983).

    Article  CAS  PubMed  Google Scholar 

  136. Shah, S. A., Page, C. P. & Pitchford, S. C. Platelet–eosinophil interactions as a potential therapeutic target in allergic inflammation and asthma. Front. Med. 4, 129 (2017).

    Article  Google Scholar 

  137. Sakai, T. et al. Eosinophils may be involved in thrombus growth in acute coronary syndrome. Int. Heart J. 50, 267–277 (2009).

    Article  PubMed  Google Scholar 

  138. Yamaji, K. et al. Association of localized hypersensitivity and in-stent neoatherosclerosis with the very late drug-eluting stent thrombosis. PLoS ONE 9, e113870 (2014).

    Article  PubMed  PubMed Central  Google Scholar 

  139. Riegger, J. et al. Histopathological evaluation of thrombus in patients presenting with stent thrombosis. A multicenter European study: a report of the prevention of late stent thrombosis by an interdisciplinary global European effort consortium. Eur. Heart J. 37, 1538–1549 (2016).

    Article  PubMed  Google Scholar 

  140. Mansiroglu, A. K., Sincer, I., Cosgun, M. & Gunes, Y. Dating thrombus organization with eosinophil counts in deep venous thrombosis. J. Vasc. Surg. Venous Lymphat. Disord. 9, 874–880 (2021).

    Article  PubMed  Google Scholar 

  141. Kulahcioglu, S. et al. Eosinophil-to-monocyte ratio as a candidate for a novel prognostic marker in acute pulmonary embolism: is it a consumptive mechanism? Anatol. J. Cardiol. 26, 717–724 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  142. Scheitz, J. F., Nolte, C. H., Doehner, W., Hachinski, V. & Endres, M. Stroke–heart syndrome: clinical presentation and underlying mechanisms. Lancet Neurol. 17, 1109–1120 (2018).

    Article  PubMed  Google Scholar 

  143. Lo, E. H., Dalkara, T. & Moskowitz, M. A. Mechanisms, challenges and opportunities in stroke. Nat. Rev. Neurosci. 4, 399–415 (2003).

    Article  CAS  PubMed  Google Scholar 

  144. Palasubramaniam, J., Wang, X. & Peter, K. Myocardial infarction — from atherosclerosis to thrombosis. Arterioscler. Thromb. Vasc. Biol. 39, e176–e185 (2019).

    Article  CAS  PubMed  Google Scholar 

  145. Heusch, G. & Gersh, B. J. The pathophysiology of acute myocardial infarction and strategies of protection beyond reperfusion: a continual challenge. Eur. Heart J. 38, 774–784 (2017).

    CAS  PubMed  Google Scholar 

  146. Hori, Y. S., Kodera, S., Sato, Y. & Shiojiri, T. Eosinopenia as a predictive factor of the short-term risk of mortality and infection after acute cerebral infarction. J. Stroke Cerebrovasc. Dis. 25, 1307–1312 (2016).

    Article  PubMed  Google Scholar 

  147. Juceviciute, N., Mikuzis, P. & Balnyte, R. Absolute blood eosinophil count could be a potential biomarker for predicting haemorrhagic transformation after intravenous thrombolysis for acute ischaemic stroke. BMC Neurol. 19, 127 (2019).

    Article  PubMed  PubMed Central  Google Scholar 

  148. Yu, S. et al. Eosinophil-to-monocyte ratio is a potential biomarker in the prediction of functional outcome among patients with acute ischemic stroke. BMC Neurosci. 22, 8 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  149. Yang, D. et al. Dynamic decrease in eosinophil after intravenous thrombolysis predicts poor prognosis of acute ischemic stroke: a longitudinal study. Front. Immunol. 12, 709289 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  150. Chen, Y. et al. Eosinophil-to-monocyte ratio is a potential predictor of prognosis in acute ischemic stroke patients after intravenous thrombolysis. Clin. Interv. Aging 16, 853–862 (2021).

    Article  PubMed  PubMed Central  Google Scholar 

  151. Fan, L., Gui, L., Chai, E. Q. & Wei, C. J. Routine hematological parameters are associated with short- and long-term prognosis of patients with ischemic stroke. J. Clin. Lab. Anal. 32, e22244 (2018).

    Article  PubMed  Google Scholar 

  152. Gunes, M. Is neutrophil/eosinophil ratio at admission a prognostic marker for in-hospital mortality of acute ischemic stroke? J. Stroke Cerebrovasc. Dis. 29, 104999 (2020).

    Article  PubMed  Google Scholar 

  153. Sundstrom, J. et al. Eosinophil cationic protein, carotid plaque, and incidence of stroke. Stroke 48, 2686–2692 (2017).

    Article  PubMed  Google Scholar 

  154. Watts, S. W., Flood, E. D., Garver, H., Fink, G. D. & Roccabianca, S. A new function for perivascular adipose tissue (PVAT): assistance of arterial stress relaxation. Sci. Rep. 10, 1807 (2020).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  155. Ailawadi, G. et al. Smooth muscle phenotypic modulation is an early event in aortic aneurysms. J. Thorac. Cardiovasc. Surg. 138, 1392–1399 (2009).

    Article  PubMed  PubMed Central  Google Scholar 

  156. Crosas-Molist, E. et al. Vascular smooth muscle cell phenotypic changes in patients with Marfan syndrome. Arterioscler. Thromb. Vasc. Biol. 35, 960–972 (2015).

    Article  CAS  PubMed  Google Scholar 

  157. Withers, S. B. et al. Eosinophils are key regulators of perivascular adipose tissue and vascular functionality. Sci. Rep. 7, 44571 (2017).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  158. Langenskiold, M., Smidfelt, K., Nordanstig, J., Bergstrom, G. & Tivesten, A. Leukocyte subsets and abdominal aortic aneurysms detected by screening in men. J. Intern. Med. 288, 345–355 (2020).

    Article  CAS  PubMed  Google Scholar 

  159. Harris, C., Croce, B. & Cao, C. Type A aortic dissection. Ann. Cardiothorac. Surg. 5, 256 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  160. Harris, C. G., Croce, B. & Tian, D. H. Type B aortic dissection. Ann. Cardiothorac. Surg. 3, 339 (2014).

    PubMed  PubMed Central  Google Scholar 

  161. Shao, Y. et al. Impacts of eosinophil percentage on prognosis acute type A aortic dissection patients. BMC Cardiovasc. Disord. 22, 146 (2022).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  162. Qin, X. et al. The role of peripheral blood eosinophil counts in acute Stanford type A aortic dissection patients. Front. Surg. 9, 969995 (2022).

    Article  PubMed  PubMed Central  Google Scholar 

  163. Zhao, K. et al. Peripheral eosinophil count is associated with the prognosis of patients with type B aortic dissection undergoing endovascular aortic repair: a retrospective cohort study. J. Am. Heart Assoc. 11, e027339 (2022).

    Article  PubMed  PubMed Central  Google Scholar 

  164. Miyata, J. et al. 12/15-Lipoxygenase regulates IL-33-induced eosinophilic airway inflammation in mice. Front. Immunol. 12, 687192 (2021).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  165. Miyata, J. et al. Dysregulated metabolism of polyunsaturated fatty acids in eosinophilic allergic diseases. Prostaglandins Other Lipid Mediat. 150, 106477 (2020).

    Article  CAS  PubMed  Google Scholar 

  166. Masterson, J. C. et al. CCR3 blockade attenuates eosinophilic ileitis and associated remodeling. Am. J. Pathol. 179, 2302–2314 (2011).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  167. Miyata, J. et al. Dysregulated synthesis of protectin D1 in eosinophils from patients with severe asthma. J. Allergy Clin. Immunol. 131, 353–360 (2013).

    Article  CAS  PubMed  Google Scholar 

  168. Metcalfe, D. D. et al. Biomarkers of the involvement of mast cells, basophils and eosinophils in asthma and allergic diseases. World Allergy Organ. J. 9, 7 (2016).

    Article  PubMed  PubMed Central  Google Scholar 

  169. Johansson, M. W. Activation states of blood eosinophils in asthma. Clin. Exp. Allergy 44, 482–498 (2014).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  170. Johansson, M. W. et al. Platelet activation, P-selectin, and eosinophil beta1-integrin activation in asthma. Am. J. Respir. Crit. Care Med. 185, 498–507 (2012).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  171. Lingblom, C., Andersson, J., Andersson, K. & Wenneras, C. Regulatory eosinophils suppress T cells partly through galectin-10. J. Immunol. 198, 4672–4681 (2017).

    Article  CAS  PubMed  Google Scholar 

  172. Pincus, S. H., Schooley, W. R., DiNapoli, A. M. & Broder, S. Metabolic heterogeneity of eosinophils from normal and hypereosinophilic patients. Blood 58, 1175–1181 (1981).

    Article  CAS  PubMed  Google Scholar 

  173. Li, W., McIntyre, T. M. & Silverstein, R. L. Ferric chloride-induced murine carotid arterial injury: a model of redox pathology. Redox Biol. 1, 50–55 (2013).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  174. Uderhardt, S. et al. Enzymatic lipid oxidation by eosinophils propagates coagulation, hemostasis, and thrombotic disease. J. Exp. Med. 214, 2121–2138 (2017).

    Article  CAS  PubMed  PubMed Central  Google Scholar 

  175. Blankenhorn, D. H. & Stern, D. Calcification of the coronary arteries. Am. J. Roentgenol. Radium Ther. Nucl. Med. 81, 772–777 (1959).

    CAS  PubMed  Google Scholar 

  176. Libby, P. Murine ‘model’ monotheism: an iconoclast at the altar of mouse. Circ. Res. 117, 921–925 (2015).

    Article  CAS  PubMed  Google Scholar 

Download references

Acknowledgements

The authors thank C. Swallom (Brigham and Women’s Hospital, Boston, MA, USA) for editorial assistance with the manuscript before submission. The authors received support from the Hainan Province Science and Technology special fund (ZDYF2020214 to J.G.); the National Natural Science Foundation of China (82300278 to J.X., 81770487, 91939107 and 82170440 to J.G. and 82170234 to C.Y.); the National Natural Science Foundation of China Incubation Project of Guangdong Provincial People’s Hospital (KY0120220041 to J.X.); the National Science Fund for Distinguished Young Scholars of Hainan Medical University (JBGS202104 to J.G.); the National Heart, Lung and Blood Institute (HL151627, HL157073, HL166538 and HL170000 to G.-P.S. and HL134892 and HL163099 to P.L.) and the National Institute of Neurological Disorders and Stroke (AG063839 to G.-P.S.).

Author information

Author notes

  1. These authors contributed equally: Junyan Xu, Junli Guo.

Authors and Affiliations

  1. Department of Cardiology, Guangdong Provincial People’s Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, China

    Junyan Xu & Tianxiao Liu

  2. Key Laboratory of Emergency and Trauma of Ministry of Education, Hainan Medical University, Haikou, China

    Junyan Xu & Junli Guo

  3. Hainan Provincial Key Laboratory for Tropical Cardiovascular Diseases Research, Institute of Cardiovascular Research of the First Affiliated Hospital, Hainan Medical University, Haikou, China

    Junli Guo

  4. Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA, USA

    Tianxiao Liu, Chongzhe Yang, Zhaojie Meng, Peter Libby & Guo-Ping Shi

  5. Department of Geriatrics, National Key Clinical Specialty, Guangzhou First People’s Hospital, Guangzhou Medical University, Guangzhou, China

    Chongzhe Yang

  6. Department of Cardiology, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, China

    Jinying Zhang

Authors
  1. Junyan Xu
    View author publications

    You can also search for this author in PubMed Google Scholar

  2. Junli Guo
    View author publications

    You can also search for this author in PubMed Google Scholar

  3. Tianxiao Liu
    View author publications

    You can also search for this author in PubMed Google Scholar

  4. Chongzhe Yang
    View author publications

    You can also search for this author in PubMed Google Scholar

  5. Zhaojie Meng
    View author publications

    You can also search for this author in PubMed Google Scholar

  6. Peter Libby
    View author publications

    You can also search for this author in PubMed Google Scholar

  7. Jinying Zhang
    View author publications

    You can also search for this author in PubMed Google Scholar

  8. Guo-Ping Shi
    View author publications

    You can also search for this author in PubMed Google Scholar

Contributions

J.X., J.G., T.L., Z.M., J.Z. and G.-P.S. researched data for the article. J.X., J.G. and G.-P.S. wrote the manuscript. J.X., J.G., C.Y., P.L., J.Z. and G.-P.S. substantially contributed to discussion of content. J.X., J.G., P.L. and G.-P.S. reviewed or edited the manuscript before submission.

Corresponding authors

Correspondence to Jinying Zhang or Guo-Ping Shi.

Ethics declarations

Competing interests

The authors declare no competing interests.

Peer review

Peer review information

Nature Reviews Cardiology thanks Daniela Cihakova, Norbert Gerdes, Sumanth Prabhu, Konstantin Stark and the other, anonymous, reviewer(s) for their contribution to the peer review of this work.

Additional information

Publisher’s note Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Supplementary information

Rights and permissions

Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.

Reprints and permissions

About this article

Check for updates. Verify currency and authenticity via CrossMark

Cite this article

Xu, J., Guo, J., Liu, T. et al. Differential roles of eosinophils in cardiovascular disease. Nat Rev Cardiol (2024). https://doi.org/10.1038/s41569-024-01071-5

Download citation

  • Accepted:

  • Published:

  • DOI: https://doi.org/10.1038/s41569-024-01071-5

Search

Advanced search

Quick links

Nature Briefing

Sign up for the Nature Briefing newsletter — what matters in science, free to your inbox daily.

Get the most important science stories of the day, free in your inbox. Sign up for Nature Briefing