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. Author manuscript; available in PMC: 2019 Jan 1.
Published in final edited form as: Kidney Int. 2017 Jul 21;93(1):81–94. doi: 10.1016/j.kint.2017.04.033

Fig. 8. A proposed model depicting the molecular mechanism by which AMPK regulates actin dynamics, MRTF-A nuclear translocation, and fibroblast activation.

Fig. 8

Under normal condition, cofilin severs and depolymerizes F-actin into G-actin, and cytoplasmic G-actin associates and retains MRTF-A in the cytoplasm. In response to injury, activated AMPK directly phosphorylates cofilin, which promotes G-actin to F-actin polymerization. Lower G-actin concentration results in releases of MRTF-A from binding to G-actin, which enters into the nucleus and induces fibroblast activation.