Prevention of Fibrosis and Pathological Cardiac Remodeling by Salinomycin

Long Noncoding RNAs in Pathological Cardiac Remodeling.

A novel long noncoding RNA Chaer acts as noncoding epigenetic regulator at the onset of cardiac hypertrophy and enables an improved understanding about the complex mechanisms in cardiovascular disease.

Editorial: Cardiac Remodeling: New Insights in Physiological and Pathological Adaptations

PDE1C deficiency antagonizes pathological cardiac remodeling and dysfunction.

Cyclic nucleotide phosphodiesterase 1C (PDE1C) represents a major phosphodiesterase activity in human myocardium, but its function in the heart remains unknown. Using genetic and pharmacological approaches, we studied the expression, regulation, function, and underlying mechanisms of PDE1C in the pathogenesis of cardiac remodeling and dysfunction. PDE1C expression is up-regulated in mouse and h...

Requirement of protein kinase D1 for pathological cardiac remodeling.

The adult heart responds to biomechanical stress and neurohormonal signaling by hypertrophic growth, accompanied by fibrosis, diminished pump function, and activation of a fetal gene program. Class II histone deacetylases (HDACs) suppress stress-dependent remodeling of the heart via their association with the MEF2 transcription factor, an activator of heart disease. Protein kinase D (PKD) is a ...

Beta-adrenoceptor signaling pathways mediate cardiac pathological remodeling.

Beta-adrenoceptors (ARs), members of the G protein-coupled receptor (GPCR) superfamily, play a key role in the rapid regulation of myocardial function. Meanwhile, chronic catecholamine stimulation of adrenoceptors has been proved to be involved in the adverse myocardial remodeling, including cardiac hypertrophy, fibrosis, and apoptosis, which finally develop into heart failure. In the clinical ...