Target intelligence / Profile preview

Myofibroblast differentiation suppression

01

Overview

Myofibroblast differentiation suppression refers to pharmacological or genetic interventions aimed at preventing or reversing the conversion of precursor cells (typically fibroblasts) into myofibroblasts. Myofibroblasts are characterized by the expression of markers such as α-smooth muscle actin and contribute to tissue fibrosis through extracellular matrix production and tissue contractility. This process is often driven by TGF-β1 and involves multiple signaling pathways (MAPK, AMPK, Hedgehog, VEGF, NOX4-derived ROS, and others). Inhibition of myofibroblast differentiation is being actively researched as a therapeutic concept to treat fibrotic diseases and reduce pathological tissue remodeling, but it is not a specific single molecular target, receptor, enzyme, or protein.

Other names
Myofibroblast transdifferentiation inhibitionInhibition of myofibroblast activationSuppression of fibroblast-to-myofibroblast transition
02

Mechanism of action

Inhibition of TGF-β1–induced signaling; Suppression of Hedgehog (Hh) and VEGF signaling; AMPK activation; Inhibition of mTOR signaling; Inhibition of mitochondrial oxidative phosphorylation (OXPHOS)

03

Biological functions

Fibrosis regulationTissue remodelingWound healingExtracellular matrix production
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Disease associations

Fibrosis (e.g., lung, liver, kidney, skin)Cancer (tumor microenvironment immunosuppression)Cardiovascular diseaseOther chronic fibroproliferative diseases
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Safety considerations

Potential impairment of normal wound healing and tissue repairOff-target modulation of TGF-β and immune pathways, with risk of abnormal immune responsesUnintended inhibition of mitochondrial function (e.g., OXPHOS)
06

Interacting drugs

Itraconazole

5 more in the full profile.

07

Biomarkers

Alpha-smooth muscle actin (α-SMA) reductionDecreased collagen type I expressionChanges in TGF-β signaling pathway activity

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