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Myocardial fibrosis is characterized by the excessive accumulation of collagenous scar tissue within the myocardium, leading to increased ventricular stiffness, reduced contractility, and increased risk of arrhythmias and heart failure. It is a consequence of various cardiac insults including ischemia, pressure/volume overload, genetic disorders, and inflammation. While not a direct 'target' in the traditional sense, it represents a pathological process that can be influenced by therapies aimed at managing underlying conditions and potentially by emerging antifibrotic drugs.
Indirectly targeted through management of underlying conditions (e.g., hypertension, ischemia); direct antifibrotic therapies targeting TGF-β signaling are under investigation.
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