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In turn, these compromised mitochondria produce excess ROS, which further stimulates pro-inflammatory gene expression through MAPK and NF-B signaling, creating a self-reinforcing feedback loop that amplifies the inflammatory cytokines response

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Thymosin 4 binds and alters cytoskeletal actin filaments by sequestering actin monomers, influencing actin filament assembly and regulating migration of various cell types including endothelial cells, myocardial cells, and epicardial progenitors

[DOI] [Google Scholar] 102.Kaya C., Ashraf M., Alyemeni M.N., Ahmad P

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