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