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

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

Lanifibranor attenuates TGF-β1-driven cardiac fibrosis by combining antifibrotic effects with metabolic and functional improvements in human models.

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.

Irisin/Integrin αVβ5/AMPK Signaling in Cardiac Fibrosis: Molecular Mechanisms and Therapeutic Potential

Cardiac fibrosis is a major pathological feature of several cardiovascular diseases and is characterized by excessive extracellular matrix deposition, leading to ventricular stiffening, impaired cardiac function, and ultimately heart failure. Despite its substantial clinical burden, therapies specifically targeting the...

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...

Endothelial S1PR3 downregulation exacerbates pressure overload-induced cardiac remodeling by promoting fibrosis and inflammation.

Glucose-dependent insulinotropic polypeptide receptor agonism improves heart failure with antifibrosis through Akt-dependent nitric oxide signaling

Cardiac fibrosis is a pathological remodeling process that contributes to the development and progression of heart failure. Although glucose-dependent insulinotropic polypeptide (GIP) may exert antifibrotic effects, how GIP receptor activation regulates cardiac fibrogenesis and modulates cardiac function in heart failu...