Target intelligence / Profile preview

Fibroblast apoptosis

Molecular classification
Other
01

Overview

Fibroblast apoptosis is a critical biological process involving the programmed cell death of fibroblast cells, which is essential for the resolution of normal wound healing and the prevention of excessive tissue scarring (PMID: 24041640). In healthy tissue repair, fibroblasts proliferate and produce extracellular matrix (ECM) but are eventually cleared via apoptosis once the wound is closed; however, in chronic fibrotic diseases like idiopathic pulmonary fibrosis (IPF) and systemic sclerosis, these cells become resistant to apoptosis (PMID: 31362758). This resistance leads to the persistence of activated myofibroblasts, resulting in continuous ECM deposition, organ stiffening, and functional failure. Therapeutic interventions often aim to restore or induce apoptosis in these pathologically activated cells by targeting anti-apoptotic proteins like BCL-2 or inhibiting pro-survival signaling pathways such as TGF-beta and PI3K/Akt (PMID: 28834927). While drugs like Nintedanib and Pirfenidone are used to manage fibrosis, newer strategies specifically look to sensitize fibroblasts to apoptotic triggers to potentially reverse established tissue damage (PMID: 25184131).

Other names
Programmed cell death of fibroblastsMyofibroblast apoptosisFibroblast programmed cell death
02

Mechanism of action

Induction of programmed cell death in pathologically activated fibroblasts or myofibroblasts to resolve excessive extracellular matrix production and promote the regression of fibrotic tissue.

03

Biological functions

ApoptosisTissue remodelingWound healingExtracellular matrix homeostasisResolution of inflammation
04

Disease associations

Idiopathic pulmonary fibrosisSystemic sclerosisLiver cirrhosisCancer (Cancer-associated fibroblasts)Hypertrophic scarringChronic kidney disease
05

Safety considerations

Impairment of physiological wound healingPotential for non-specific systemic apoptosisTissue atrophyIncreased risk of infection due to disrupted tissue barriers
06

Interacting drugs

Nintedanib

5 more in the full profile.

07

Biomarkers

Cleaved Caspase-3Alpha-smooth muscle actin (α-SMA) reductionTUNEL-positive fibroblastsAnnexin V bindingPro-collagen I C-terminal propeptide (PICP)

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