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. Author manuscript; available in PMC: 2019 Jun 24.
Published in final edited form as: J Med Chem. 2019 Apr 18;62(9):4350–4369. doi: 10.1021/acs.jmedchem.8b01772

Figure 1.

Figure 1

The fibroblast-to-myofibroblast transition is tightly regulated by Rho/MRTF/SRF signaling. Both soluble and mechanical stimuli promote MRTF nuclear translocation in fibroblasts. In the resting state, actin is not polymerized, and MRTF is bound to G-actin and sequestered into the cytoplasm. When stress fibers form in response to these stimuli, G-actin polymerizes into F-actin and MRTF is released. This allows MRTF to translocate into the nucleus via binding to importins followed by MRTF/importin/nuclear pore complex (NPC) formation. The MRTF/SRF coactivator complex increases ECM and pro-fibrotic gene expression, contributing to the fibroblast-to-myofibroblast transition.