Lanifibranor (IVA-337) - a pan-PPAR agonist suppresses TGF-β1-induced cardiac fibrosis and rescues cardiomyocyte function

The dual PPAR-α/δ agonist elafibranor attenuates TGF-β1-induced cardiac fibrosis through redox-metabolic and bioenergetic reprogramming in human cardiac models

Hypertrophic cardiomyocytes promote cardiac fibrosis through paracrine secretion of ketoisoleucine in pressure-overloaded hearts

Cardiac fibrosis is a critical pathological feature that drives pressure overload (PO)-induced heart failure (HF). This process involves a complex intercellular crosstalk between cardiac fibroblasts (CFs) and cardiomyocytes. Cardiomyocyte hypertrophy is a compensatory response to PO and undergoes metabolic reprogra...

Ellagic acid attenuates myocardial fibrosis by suppressing Bmi1-mediated inhibition of the p53/p21 pathway in cardiac fibroblasts.

Eriodictyol targets the ubiquitination/phosphorylation of apoptosis signal-regulating kinase 1 and alleviates pressure-overload induced myocardial fibrosis in mice.

BACKGROUND AND PURPOSE Myocardial fibrosis, a critical pathogenic driver of cardiovascular events, is primarily characterized by extracellular matrix deposition and cardiac fibroblast proliferation and activation. Eriodictyol (ERIO) is an extractable natural compound widely found in fruits and vegetables, possessing po...

SerpinA3 is an Endogenous TGF‐β Receptor Antagonist that Attenuates Cardiac Fibroblast Activation and Fibrotic Remodeling

ABSTRACT Background: Cardiac fibrosis is a central driver of adverse remodeling and heart failure (HF), yet effective antifibrotic therapies remain limited. SerpinA3, a member of the serine protease inhibitor family, has been implicated in cardiovascular disease, but its functional role and underlying mechanisms in car...

BET inhibitor apabetalone suppresses the fibrotic activation of cardiac fibroblasts associated with heart dysfunction.

BACKGROUND Accumulation of extracellular matrix (ECM) causes tissue fibrosis that contributes to myocardial dysfunction and heart failure (HF), yet there are no approved anti-fibrotic therapeutics that target it. Inhibitors of BET proteins (BETi) reduced fibrosis in preclinical HF models, and clinical-stage BETi, apabe...