Myocardial scar reduction

Myocardial scar reduction refers to the clinical and biological process of decreasing the volume of fibrotic tissue in the heart, typically following a myocardial infarction (MI) [PMID: 29444643]. It is not a single molecular target but a therapeutic goal achieved by modulating pathways such as the TGF-beta signaling cascade and the renin-angiotensin-aldosterone system (RAAS) [PMID: 30630134]. Following cardiac injury, fibroblasts transform into myofibroblasts, which deposit excessive extracellular matrix (ECM) proteins, leading to a permanent scar that impairs contractility and promotes heart failure [PMID: 28249114]. Drugs like ACE inhibitors and mineralocorticoid receptor antagonists are used to limit this remodeling, while experimental therapies like cardiosphere-derived cells or CRISPR-based gene editing target the active regression of existing fibrosis [PMID: 24445366]. Successful reduction of myocardial scars is monitored via imaging techniques like Late Gadolinium Enhancement (LGE) Cardiac Magnetic Resonance (CMR) [PMID: 25249136].

Other names

Cardiac scar regressionReduction of myocardial fibrosisInfarct size limitationVentricular remodeling attenuation

Reduction of myocardial scar is achieved by inhibiting the activation of myofibroblasts, suppressing the TGF-beta/Smad signaling pathway, and modulating the renin-angiotensin-aldosterone system to decrease collagen deposition and promote extracellular matrix turnover [PMID: 30630134, PMID: 28249114].