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Myocardial scar tissue is a non-contractile, collagen-rich structure that replaces functional cardiomyocytes following significant cardiac injury, most commonly myocardial infarction [1]. This process, known as replacement fibrosis, is essential for maintaining the structural integrity of the heart wall to prevent rupture, but it leads to adverse ventricular remodeling and impaired systolic and diastolic function [2]. The scar is primarily composed of cross-linked Type I and Type III collagen fibers secreted by activated myofibroblasts [3]. While the scar itself is not a single molecular target, its components and the signaling pathways driving its formation (such as the TGF-beta and RAAS pathways) are major focuses for therapeutic intervention to prevent heart failure and arrhythmias [4]. Imaging techniques like Late Gadolinium Enhancement (LGE) MRI are the gold standard for visualizing and quantifying the extent of the scar in clinical practice [5].
Modulation of fibrotic pathways including TGF-beta signaling and the renin-angiotensin-aldosterone system (RAAS), as well as diagnostic visualization through extracellular contrast agent accumulation [3, 4, 5]
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