Myofibroblast

Myofibroblasts are specialized mesenchymal cells that combine the biosynthetic capacity of fibroblasts with the contractile properties of smooth muscle cells [1]. They are defined by the de novo expression of alpha-smooth muscle actin (alpha-SMA) and are the primary effectors of extracellular matrix (ECM) deposition during tissue repair [2]. While essential for normal wound healing, the chronic presence of myofibroblasts is a central driver of organ fibrosis, leading to structural remodeling and functional failure in the lungs, liver, kidneys, and heart [3]. In the tumor microenvironment, these cells are known as cancer-associated fibroblasts (CAFs) and contribute to tumor growth, invasion, and immune evasion [4]. Pharmacological strategies targeting myofibroblasts focus on inhibiting their activation from precursor cells, blocking pro-fibrotic signaling pathways like TGF-beta, or promoting their apoptosis or senescence [5]. Current approved therapies like nintedanib and pirfenidone work by modulating these cellular activities to slow the progression of fibrotic diseases [6].

Other names

Activated fibroblastAlpha-SMA-positive fibroblastContractile fibroblastCancer-associated fibroblast (CAF)

Inhibition of TGF-beta signaling pathways, blockade of tyrosine kinase receptors (PDGFR, FGFR, VEGFR), and modulation of fibroblast-to-myofibroblast transition.