Myocardial fibrosis pathways

Myocardial fibrosis pathways constitute a network of cellular signaling events driven by myocardial injury, stress, aging, or metabolic dysfunction, leading to activation of cardiac fibroblasts, their differentiation into myofibroblasts, and subsequent deposition/enhanced remodeling of extracellular matrix proteins. Central profibrotic signaling pathways include TGF-β, RAAS, inflammatory cytokines (TNF-α, IL-6, IL-1), and downstream kinase cascades (such as p38 MAPK). These processes result in increased cardiac stiffness, impaired contractility, and ultimately heart failure. The complexity of these pathways means that clinical intervention often targets key nodes, such as renin-angiotensin signaling, TGF-β signaling, or epigenetic regulators, rather than a single molecular entity.

Other names

myocardial fibrosis signalingcardiac fibrosis pathwayscardiac fibrotic remodeling pathways

Inhibition of angiotensin II signaling; Blockade of TGF-β signaling (via antibodies, receptor antagonists, small molecules); Inhibition of fibroblast proliferation/differentiation; Modulation of inflammatory cytokine signaling; Epigenetic modification (targeting chromatin regulatory factors)