Cardiovascular Effects of Exercise

This study shows that blocking CD14 reduces arrhythmogenic cardiomyopathy in mice by decreasing inflammation and fibrosis.

This study shows that PAD4-dependent NETosis and MPO contribute to inflammation, fibrosis, and arrhythmias in ACM, with targeting these pathways improving cardiac function.

This study examines age-dependent differences in cardiac hypertrophy and regression in female mice following exercise and detraining, identifying distinct molecular pathways in young versus adult hearts.

This study identifies pro-adhesive compounds from an FDA-approved drug library that restore cell-cell adhesion in ACM patient mutations and show protective effects in a mouse model.

This study identifies metabolic defects in PKP2-deficient cardiomyocytes and shows that restoring PKP2 improves contractility and electrophysiological properties.

The paper reports the coexistence of ST-segment depression and exaggerated blood pressure response in older runners during exercise stress tests, suggesting the need for cardiovascular risk assessment in masters athletes.

This study investigates the molecular and metabolic effects of PKP2 knockdown in a guinea pig ARVC model, revealing ECM remodeling and metabolic changes associated with the disease.

The paper shows that SARS-CoV-2 Nsp1 protein mimics the effects of a PKP2 mutant by altering actomyosin cytoskeleton organization, suggesting a potential link between viral infection and ACM-like disease.

The paper identifies SORBS2 as a new susceptibility gene for arrhythmogenic right ventricular cardiomyopathy (ARVC) using zebrafish and mouse models and human patient sequencing.