A. Laimbacher

Comparison of Culture Systems for Mouse Living Myocardial Slices in Cardiac Fibrosis Research

Dysferlin is a novel regulator of COMP-positive matrifibrocytes in heart failure

Dysferlin is a stress-inducible antifibrotic regulator that limits maladaptive fibroblast differentiation and myocardial fibrosis, thereby representing a potential therapeutic target to attenuate adverse cardiac remodelling in HF.

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.

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.