Cardiac Fibrosis and Remodeling

The paper develops a computational model to simulate fibroblast signaling and fibrosis after myocardial infarction, revealing how paracrine stimuli and signaling pathways drive fibroblast phenotype dynamics.

This study investigates the role of miR-21 in hypertrophic cardiac remodeling, showing that its suppression prevents remodeling by regulating PDCD4, AP-1, and TGF-β1 signaling.

This study shows that blocking CDH11 reduces inflammation-driven fibrosis and improves cardiac function after myocardial infarction in mice.

This study shows BRD4 promotes cardiac fibrosis by dynamically targeting chromatin and activating gene expression in fibroblasts, revealing a signaling pathway involved in heart failure.

The paper identifies translational regulators of fibrogenic genes in human cardiac fibroblasts and shows their role in cardiac fibrosis through ribosome profiling and RNA-binding protein analysis.

This study investigates sex differences and stimulus-specific mechanisms in the regression of pathological cardiac hypertrophy in mouse models.

The paper examines MYOCD expression in DCM patients with and without renal disease and evaluates the effects of MYOCD silencing in a cardiorenal syndrome rat model.

This paper investigates how Hcy-induced atrial fibrosis is mediated by TRPC3 and SIRT1 interactions, showing increased fibrosis and TRPC3 expression in high-Hcy conditions.

This study shows that administering HMGB1 fragment improves cardiac function and reduces fibrosis in a hamster model of dilated cardiomyopathy by enhancing stem cell homing.