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Gandhi, Zivkovic, Østergaard and colleagues describe a bispecific antibody, HMB-001, which could be used for the prophylactic treatment of patients with genetic bleeding disorders, currently treated acutely with recombinant coagulation factor VIIa. HMB-001 can bind and accumulate endogenous FVIIa and localize it to sites of vascular injury by targeting it to the TREM-like transcript-1 receptor selectively expressed on activated platelets.
Selvakumar, Clayton et al. use a porcine model of myocardial infarction and PSC-CM transplantation and identify atrial and pacemaker-like cardiomyocytes as the cause of engraftment arrhythmias and surface marker signatures to distinguish between arrhythmogenic and non-arrhythmogenic cardiomyocytes.
Döring, van der Vorst, Yan, Neideck et al. present a non-canonical chemokine pathway involving CCL17 signaling through CCR8, which induces CCL3 expression independent of CCR4 and suppresses the functions of atheroprotective Treg cells.
Wu et al. profile the secretome of cardiac endothelial cells exposed to endoplasmic reticulum (ER) stress during acute myocardial infarction and identify CRELD2 as an angiogenic growth factor supporting infarct repair.
Fidler et al. show that anti-IL-1β treatment of atherosclerotic Ldlr-null mice with clonal expansion of Tet2-null or Jak2VF hematopoietic stem cells promotes the recruitment of fibroblast-like cells to the plaque fibrous cap, leading to cap thickening and increased plaque stability. Conversely, the removal of fibroblast-like cells during atherosclerosis progression results in reduced fibrous cap formation in mice receiving anti-IL-1β antibody treatment.
Shao, Li, Liu et al. identify the GAS6–ATF3 axis as a central regulator of survival and proliferation of protective resident MerTK+ cardiac macrophages and show that GAS6 administration improves cardiac repair after ischemic–reperfusion injury in mice in an ATF3-dependent manner.
Stoffers, Wolf et al. report that, in virus-mediated myocarditis, GPR15 deficiency delays the recruitment of T cells into cardiac tissue, which impairs viral elimination and leads to delayed but also prolonged inflammation and, thus, adverse cardiac outcomes.
Lhoste et al. show that cardiometabolic and renal traits of the US population have shifted from phenotypes with high blood pressure and high cholesterol toward poor kidney function, hyperglycemia and severe obesity.
Bradford, Zhang and colleagues generate a mouse model harboring a mutation that impacts PKP2 splicing and show that one-time administration of AAV-PKP2 in neonatal mice could restore PKP2 and prevent the onset of key pathological features of arrhythmogenic right ventricular cardiomyopathy, and one-time administration in adult mice could rescue the phenotype and prevent sudden death up to 4 months post treatment.
Kyriakopoulou et al. report that adeno-associated virus-mediated delivery of PKP2 in PKP2c.2013delC/WT induced pluripotent stem cell-derived cardiomyocytes and heterozygous Pkp2c.1755delA knock-in mice restores cardiomyocyte junctions, enhances cardiac function and mitigates arrhythmogenic substrates leading to arrhythmogenic cardiomyopathy.
Zhang et al. show that bone marrow fatty acid metabolism fuels expanded leukocyte production after myocardial infarction and, based on mouse, pig and human data, suggest that lipolysis in marrow adipocytes provides fatty acids to hematopoietic stem cells.
Nishino et al. show how maternal diabetes leads to epigenetic changes in cardiac and pharyngeal progenitor subsets with anteroposterior patterning and retinoic acid signaling dysregulation, revealing how environmental factors can cause birth defects.
Romero-Becerra et al. report that stress kinases p38γ and p38δ are activated in ventricles of old mice and in arrhythmogenic conditions, and they demonstrate that p38γ/δ -driven phosphorylation of RyR2 and SAP97 is a trigger for ventricular fibrillation.
Metabolism can influence gene expression through histone modifications. Using a mouse model of the inborn error of metabolism propionic acidaemia, Park et al. show how raised propionate levels produce epigenetic actions that impact cardiac function.
Zhang et al. report that alkaline ceramidase 1–mediated ceramide degradation in platelets alleviated platelet-involved vascular inflammation and abdominal aortic aneurysm formation but without affecting hemostasis and thrombosis.
By single-cell mass cytometry and adoptive transfer of B cell subtypes in mice, Pattarabanjird et al. show that human CD24hi circulating marginal zone B cells produce IgM to atherosclerosis antigens and confer atheroprotection. Blocking CD24 increased vascular inflammation in hyperlipidemic humanized mice.
Patterson, Firulyova, et al. report that TREM2 is a key regulator of foamy macrophage differentiation. Myeloid-specific deletion of Trem2 caused increased macrophage susceptibility to cholesterol-mediated toxicity and cell death and significantly attenuated atherosclerotic plaque progression in mice.
Abd Alla et al. identify bublin coiled-coil protein (BBLN) as a factor upregulated in unrepaired hearts of patients with tetralogy of Fallot, and show that this protein binds to and controls the function of calcium/calmodulin-dependent protein kinase II delta (CAMK2D). Overexpression of BBLN in mice induced pathological cardiac remodeling, which was precluded when the interaction of BBLN with CAMK2D was prevented or upon CAMK2D downregulation.
The results of EMPATROPISM-FE, a post hoc analysis of the EMPA-TROPISM trial performed by Angermann et al., suggest that the beneficial effects of empagliflozin treatment in heart failure populations may be related to changes in iron metabolism.