Myocardial infarction causes endoplasmic reticulum (ER) stress, thereby triggering the release of a set of poorly defined growth factors. A study shows that the growth factor CRELD2 is secreted in response to ER stress and is required for preserving heart function after myocardial infarction in mice.
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References
Oh-hashi, K., Kunieda, R., Hirata, Y. & Kiuchi, K. Biosynthesis and secretion of mouse cysteine-rich with EGF-like domains 2. FEBS Lett. 585, 2481–2487 (2011). This paper shows that CRELD2 residing inside the ER might be secreted.
Kern, P. et al. Creld2 function during unfolded protein response is essential for liver metabolism homeostasis. FASEB J. 35, e21939 (2021). This paper describes Creld2-deficient mice.
Wu, X., Reboll, M. R., Korf-Klingebiel, M. & Wollert, K. C. Angiogenesis after acute myocardial infarction. Cardiovasc. Res. 117, 1257–1273 (2021). A review article on angiogenesis after myocardial infarction.
Ren, J., Bi, Y., Sowers, J. R., Hetz, C. & Zhang, Y. Endoplasmic reticulum stress and unfolded protein response in cardiovascular diseases. Nat. Rev. Cardiol. 18, 499–521 (2021). A review article on ER stress in cardiovascular diseases.
Chen, X. & Cubillos-Ruiz, J. R. Endoplasmic reticulum stress signals in the tumour and its microenvironment. Nat. Rev. Cancer 21, 71–88 (2021). A review article on ER stress in the tumor microenvironment.
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This is a summary of: Wu, X. et al. Cysteine-rich with EGF-like domains 2 (CRELD2) is an endoplasmic reticulum stress-inducible angiogenic growth factor promoting ischemic heart repair. Nat. Cardiovas. Res. https://doi.org/10.1038/s44161-023-00411-x (2024).
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Angiogenic factor induced by ER stress promotes tissue repair after myocardial infarction. Nat Cardiovasc Res 3, 108–109 (2024). https://doi.org/10.1038/s44161-024-00430-2
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DOI: https://doi.org/10.1038/s44161-024-00430-2