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doi: 10.1016/j.lfs.2020.118090 164 LinHHTsengCYYuPRHoHYHsuCCChenJH
This mechanism involves: Sequestration of monomeric actin (G-actin) to prevent premature polymerization Promotion of actin polymerization into functional microfilaments (F-actin) when needed Enhanced cellular migration through cytoskeletal reorganization Facilitation of cell shape changes necessary for wound healing Research indicates TB-500 may work with the Arp2/3 protein complex to orchestrate actin polymerization, though this mechanism requires further clarification[4]
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It has been proposed that mitochondrial NADPH not only affects the mitochondrial redox state but could also, through the action of substrate shuttles, increase NADPH in the cytosol [41,42,43,44]
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