Figure 3.

The myofibroblast in the center of attention. Anti-fibrotic therapies can be designed to interfere with the extracellular chemical and mechanical factors that lead to myofibroblast formation from a variety of different precursors. Alternatively, one might interfere with intracellular signaling pathways, transcription regulators, and epigenetic mechanisms that specifically modulate myofibroblast differentiation. Other potential anti-fibrotic targets are specific features of the differentiated myofibroblast, such as α-SMA in the contractile apparatus, specific integrins, and ECM proteins. Other strategies aim to induce myofibroblast regression and/or apoptosis

(modified and reproduced with permission from the study by Hinz and Gabbiani¹⁶¹).