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By integrating DNA genotype and RNA sequencing data from human samples, d’Escamard et al. identify a gene regulatory co-expression supernetwork that plays an important role in fibromuscular dysplasia, a poorly understood disease affecting 3–5% of adult females.
Goumenaki et al. uncover that during zebrafish cardiac regeneration, MyD88 signaling promotes the inflammatory response to injury and attenuates the endocardial-mediated fibrotic response.
Joshi et al. show that γ-protocadherins suppress the anti-inflammatory KLF2 and KLF4 pathway and that targeting them is a viable therapeutic strategy to protect against atherosclerosis.
Yu Shi et al. show that the citric acid cycle metabolite α-ketoglutarate promotes cardiomyocyte proliferation during heart development and promotes heart regeneration after myocardial infarction.
Boulgakoff et al. show that during cardiac regeneration, ventricular trabeculae participate in the repair of the contractile myocardium resulting in an excessive production of immature Purkinje fibers forming a hyperplastic PF network and altered ventricular conduction.
Sarig and Tzahor et al. show that the multiple sclerosis drug glatiramer acetate improves cardiac function and reduces scar area in rodent models of acute myocardial infarction and ischemic heart failure.
Vyas et al. show that epicardial adipose tissue is a reservoir for a subpopulation of tissue-resident memory T cells that can increase the vulnerability of the heart to atrial fibrillation.
Using engineered cardiac tissues, Fleischer, Nash et al. found that patients with lupus-mediated cardiac damage have unique autoantibodies that can independently alter tissue function. They also identified autoantibodies associated with heart injury.
Shetty et al. report that a favorable cardiovascular risk factor profile may partially offset the risk of heart failure and atrial fibrillation among carriers of high-proportion spliced-in titin truncating variants.
Sivaraj, Majev et al. demonstrate that the inactivation of Lats2 in endothelial cells triggers the upregulation of serum response factor and endothelial-to-mesenchymal transition, leading to myofibroblast formation, bone marrow fibrosis, osteosclerosis, impaired bone marrow function and extramedullary hematopoiesis.
Although heart failure with preserved ejection fraction has a normal-looking contraction, under an electron microscope the muscle looks abnormal, with disrupted contracting proteins and mitochondria and excess fat, particularly in the most obese patients.
Z. Liu, Y. Liu and Z. Yu et al. discovered a subtype of valve interstitial cells underneath the valve endothelial cells sensing unidirectional flow. These cells express high levels of APOE, which is responsible for JAG1–NOTCH2-mediated fetal elastogenesis.
Hartman et al. use mouse models of cardiac function to show that aficamten decreases the availability of myosin heads for contraction during systole, attenuating a primary driver of hypertrophic cardiomyopathy pathophysiology.
Elezaby et al. show that cardiac troponin I interacts with mitochondrial ATP synthase to increase ATPase activity. Disrupting this interaction reduces cardiac damage following transient ischemia.
Bayer et al. show that CD8+ T cells contribute to the adverse cardiac effect of doxorubicin administration, promoting fibroblast activation and inflammation through a mechanism dependent on IFNγ and the degranulation of granzyme B.
Haykin et al. show that activation of the brain’s reward system modulates adrenergic input to the liver and complement component 3 transcription, affecting vascularization and improving cardiac recovery after acute myocardial infarction.
Prabhakar et al. demonstrate in rats with mitomycin C-caused pulmonary veno-occlusive disease activation of protein kinase R (PKR) and the integrated stress response (ISR), leading to the depletion of VE-cadherin and RAD51 from endothelial junctions, endothelial barrier disruption and vascular remodeling. Inhibiting the PKR–ISR axis protects against mitomycin C-induced endothelial damage.
Deng et al. show that endothelial cells respond to high fluid shear stress by KLF2-mediated induction of the BMP–Smad1/5 pathway inhibitor BMPER, resulting in outward vessel remodeling, and apply this knowledge to develop an approach that improves vessel remodeling in mouse models of diabetes.
Using bulk heart transcriptomics of rat models of right and left ventricle failure, Jurida et al. examined transcriptional changes in cardiomyocytes during the progression of heart failure and the overlap with transcriptomics from humans with chronic thromboembolic pulmonary hypertension (CTEPH), identifying more than 50 genes whose expression levels correlate with the severity of right heart disease.