Cardiac fibrosis is a key pathological feature of both heart failure and adverse ventricular remodeling following myocardial infarction (MI). It contributes to diastolic and systolic dysfunction, arrhythmogenesis, and long-term morbidity. While traditional pharmacological agents such as the renin angiotensin-aldosterone system (RAAS) inhibitors exert indirect antifibrotic effects, recent advances have identified novel pathways and agents that may allow for direct modulation of fibrotic remodeling. This has opened the door to a new therapeutic era focused on disease modification at the myocardial tissue level.
(2025). Rewriting The Scar: Emerging Antifibrotic Therapies in Heart Failure and Post-MI Remodeling. Cardiovascular Research Prove Journal, 9(1), -. doi: 10.21608/cvrepj.2025.438170
MLA
. "Rewriting The Scar: Emerging Antifibrotic Therapies in Heart Failure and Post-MI Remodeling", Cardiovascular Research Prove Journal, 9, 1, 2025, -. doi: 10.21608/cvrepj.2025.438170
HARVARD
(2025). 'Rewriting The Scar: Emerging Antifibrotic Therapies in Heart Failure and Post-MI Remodeling', Cardiovascular Research Prove Journal, 9(1), pp. -. doi: 10.21608/cvrepj.2025.438170
VANCOUVER
Rewriting The Scar: Emerging Antifibrotic Therapies in Heart Failure and Post-MI Remodeling. Cardiovascular Research Prove Journal, 2025; 9(1): -. doi: 10.21608/cvrepj.2025.438170
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