Target intelligence / Profile preview

Suppression of fibrosis

01

Overview

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.

Other names
Anti-fibrotic effectInhibition of fibrogenesisFibrosis suppressionReversal of fibrosis
02

Mechanism of action

Not applicable as this is a biological process or therapeutic outcome, not a specific molecular target.

03

Biological functions

Extracellular matrix organizationWound healingTissue remodelingMyofibroblast differentiation
04

Disease associations

Idiopathic pulmonary fibrosisLiver cirrhosisChronic kidney diseaseSystemic sclerosisCardiac fibrosisNonalcoholic steatohepatitis (NASH)
05

Safety considerations

Impaired normal wound healingPotential for systemic toxicity if essential tissue remodeling is inhibitedRisk of bleeding or tissue fragility
06

Biomarkers

Pro-collagen type III N-terminal peptide (PIIINP)Matrix metalloproteinases (MMPs)Tissue inhibitors of metalloproteinases (TIMPs)Enhanced Liver Fibrosis (ELF) scoreGalectin-3

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