Fibrogenic cell

Fibrogenic cells, primarily myofibroblasts and activated hepatic stellate cells (HSCs), are the central effectors in the development of tissue fibrosis across various organs, including the liver, lungs, and kidneys (Friedman, 2008; Wynn, 2008). Upon chronic injury, these cells undergo a phenotypic transition from a quiescent state to an activated, proliferative, and contractile state (Hinz, 2010). This activation is characterized by the expression of alpha-smooth muscle actin (alpha-SMA) and the excessive production of extracellular matrix (ECM) components like collagen. The resulting accumulation of scar tissue disrupts organ architecture and eventually leads to organ failure. Therapeutic strategies targeting these cells aim to inhibit their activation, promote their reversion to a quiescent state, or induce their apoptosis to halt or reverse fibrotic progression. Drugs such as nintedanib and pirfenidone are currently utilized to manage fibrotic conditions by interfering with the signaling pathways, such as TGF-beta and PDGF, that drive fibrogenic cell activity. However, achieving cell-specific targeting remains a challenge to avoid interfering with normal wound healing processes.

Other names

MyofibroblastActivated hepatic stellate cellActivated fibroblastCollagen-producing cellActivated HSC

Inhibition of myofibroblast activation, reduction of extracellular matrix production, and promotion of fibrogenic cell apoptosis or senescence.