Myofibroblasten

Myofibroblasts (German: Myofibroblasten) are specialized contractile cells that participate in tissue repair and fibrotic processes. They combine features of fibroblasts and smooth muscle cells, notably a developed contractile apparatus and expression of alpha-smooth muscle actin (α-SMA).

Most myofibroblasts arise from resident fibroblasts that become activated by inflammatory signals, especially transforming growth factor-beta (TGF-β). Additional sources include circulating fibrocytes, pericytes, and cells undergoing epithelial-to-mesenchymal transition (EMT) or endothelial-to-mesenchymal transition (EndoMT). A characteristic marker set includes α-SMA and vimentin; ED-A fibronectin is often upregulated, and these cells produce collagen type I and III.

In wound healing, myofibroblasts generate contractile force to close wounds and secrete extracellular matrix components such as collagen and fibronectin, along with remodeling enzymes. Mechanical cues and signaling pathways such as RhoA/ROCK promote their differentiation and activity. After wound resolution, myofibroblasts typically undergo apoptosis or revert to a less active fibroblast phenotype.

Persistent activation of myofibroblasts contributes to pathological fibrosis and excessive scarring. They are implicated in fibrotic diseases of the lung, liver, kidney, and heart, and can also appear in tumor-associated stroma where they influence disease progression. Regulation is centered on TGF-β signaling, ECM mechanics, and feedback between contractility and matrix remodeling.

Therapeutic approaches aim to limit myofibroblast formation or persistence by targeting profibrotic signaling, matrix stiffness, or downstream effectors of the contractile apparatus.