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Cardiac remodeling pathways comprise a complex network of molecular and cellular signaling mechanisms that drive structural and functional changes in the heart, particularly after injury (such as myocardial infarction), chronic pressure, or volume overload. These processes involve myocyte death, hypertrophy, fibrosis, inflammation, extracellular matrix remodeling, angiogenesis, and altered metabolic activity. Pathological remodeling is central in the progression to heart failure and has become a major focus for therapeutic intervention, with multiple drug classes targeting specific aspects of these cascades. However, “cardiac remodeling pathways” is not a single molecule or receptor, but rather a collective term for multiple interlinked targets and mechanisms involved in adverse or adaptive cardiac remodeling.
Inhibition of neurohormonal signaling (e.g., angiotensin II, sympathetic activation) Anti-fibrotic action (such as TGF-β pathway inhibition) Inhibition of matrix metalloproteinases (reducing extracellular matrix remodeling) Modulation of inflammation (e.g., NF-κB inhibition) Reduction of cellular hypertrophy and apoptosis Enhancing autophagy and metabolic regulation
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