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Suppression of fibrosis is a therapeutic objective aimed at preventing or reversing the pathological accumulation of extracellular matrix (ECM) proteins, such as collagen, which leads to organ scarring and dysfunction (Wynn, 2008, J. Pathol.). It is a biological process or clinical outcome rather than a specific molecular target like a receptor or enzyme (Henderson et al., 2020, Nature). Fibrosis is a hallmark of various chronic diseases, including idiopathic pulmonary fibrosis (IPF), liver cirrhosis, and chronic kidney disease (Richeldi et al., 2017, Lancet). While numerous drugs are developed to achieve the suppression of fibrosis by targeting pathways like TGF-beta signaling or myofibroblast activation, the term itself does not refer to a discrete protein or gene (Distler et al., 2019, Nat. Rev. Rheumatol.). Consequently, this entry is classified as incorrect for a molecular target database as it lacks a specific molecular structure or binding site for pharmacological agents.
Not applicable as this is a biological process or therapeutic outcome, not a specific molecular target.
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