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Physical activity lowers the risk of cardiovascular disease and overall mortality. Research now shows that women may derive greater cardiovascular benefit from exercise than men.
Chen, Wang, Zhong and colleagues show that females derive greater cardiovascular benefits from guideline-recommended levels of physical activity and require less activity than males to see their beneficial effects.
Tan et al. identify PRDM16 as a key repressor of fibrotic switching in smooth muscle cells and show that its downregulation in atherosclerosis drives smooth muscle cells toward a synthetic fate, promoting fibrous plaques.
This study examines electrical conduction through fibrotic regions in a mouse model of arrhythmogenic cardiomyopathy. A correlative imaging approach that integrates macroscopic cardiac electrophysiology with microscale whole-heart morphological reconstructions showed that the effect of fibrosis on conduction depends on the pacing frequency.
Lin, Geng and colleagues identify a non-canonical AHR pathway that is activated by canonical AHR inhibitors, promoting the proliferation of quiescent endothelial cells with potential applications in cell therapy.
Amiad Pavlov, Heffler, et al. demonstrate that stress transmitted to the cardiomyocyte nucleus by the microtubule cage drives LMNA-associated cardiomyopathy and may represent a promising therapeutic target.
Cardiac dysfunction in diabetes is linked to metabolic stress, lipid overload and fibrosis. A study now demonstrates impaired glycogen clearance as a central disease mechanism, in which failed glycophagy drives glycogen accumulation and creates a metabolic ‘sugar trap’ that can be targeted therapeutically.
Yamazoe et al. show that B cell-derived autoantibodies contribute to the development of atrial fibrillation, suggesting that targeting the humoral immune response may represent a viable therapeutic approach.
Massively parallel reporter assays (MRPAs) are used in vascular smooth muscle cells to measure the functional effects of over 25,000 variants associated with coronary artery disease. This approach identifies regulatory variants in moderate linkage to disease-associated loci, implicating a broader spectrum of causal variants.
Mulholland et al. identify progenitor exhausted T cells, expressing intermediate levels of PD-1 (PD-1int), as a prominent source of pro-inflammatory cytokines in the murine atherosclerotic aorta and potential cellular targets driving checkpoint inhibition-elicited pro-atherosclerotic immune responses. They further demonstrate elevated levels of circulating PD-1-expressing T cells in individuals with subclinical cardiovascular disease.
Barbera et al. identify and map genetic variants that alter the characteristics of vascular smooth muscle cells and contribute to the risk of coronary artery disease.
Giardini et al. present an imaging method that combines quantitative measurements of cardiac electrophysiology with high-resolution three-dimensional structural reconstructions, enabling the detection of arrhythmogenic electrical coupling between cardiomyocytes and non-myocytes in murine hearts.
Wünnemann et al. generate a subcellular resolution spatial map of the murine heart after myocardial infarction, revealing that immune cells can infiltrate the organ through the endocardium.
Oxidative phosphorylation was considered detrimental for heart regeneration, as it produces reactive oxygen species that block cardiomyocyte proliferation by causing DNA damage. However, harnessing natural variation in the regenerative capacity of seven wild-type zebrafish strains has revealed that the activation of oxidative metabolism after proliferation is essential for cardiomyocyte maturation and successful regeneration.
Boccella, Yu and colleagues reveal that the transmembrane protein ANTXR1 regulates post-infarction fibrotic remodeling, and its inhibition blocks collagen turnover and improves heart function.
Lekkos et al. show that a metabolic switch toward oxidative phosphorylation is required for cardiomyocyte re-differentiation and heart regeneration after injury in fish.
Mellor et al. report that deficiency of GABARAPL1, an ATG8-specific linking protein, impairs diastolic function in diabetic mice. This effect can be reversed by gene delivery of the gene encoding GABARAPL1 in diabetic mice and a human organoid model of type 2 diabetes.
