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

Elafibranor mitigates TGF-β1-driven cardiac fibrosis by suppressing fibroblast activation and ECM remodelling while promoting adaptive metabolic, redox, and bioenergetic responses, supporting balanced PPAR-α/δ activation as a potential therapeutic strategy for cardiac fibrosis.

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.

ERIO is a safe, effective natural flavonoid with promising preclinical efficacy, suggesting its potential clinical translation for myocardial fibrosis and offering new therapeutic targets to prevent heart failure progression.

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

SerpinA3 functions as an endogenous inhibitor of TGF‐β signaling that restrains cardiac fibroblast activation and fibrotic remodeling and is identified as a promising therapeutic target for HF associated with pathological fibrosis.

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...