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This study is aimed at exploring the mechanisms underlying IR\u2010induced senescence using acetylation proteomics. <jats:italic>Methods.<\/jats:italic> Irradiated mouse hearts and H9C2 cells were harvested for senescence detection. Acetylation proteomics was used to investigate alterations in lysine acetylation. Atp5f1c acetylation after IR was verified using coimmunoprecipitation (Co\u2010IP). Atp5f1c lysine 55 site acetylation (Atp5f1c K55\u2010Ac) point mutation plasmids were used to evaluate the influence of Atp5f1c K55\u2010Ac on energy metabolism and cellular senescence. Deacetylation inhibitors, plasmids, and siRNA transfection were used to determine the mechanism of Atp5f1c K55\u2010Ac regulation. <jats:italic>Results.<\/jats:italic> The mice showed cardiomyocyte and cardiac aging phenotypes after IR. We identified 90 lysine acetylation sites from 70 protein alterations in the heart in response to IR. Hyperacetylated proteins are primarily involved in energy metabolism. Among them, Atp5f1c was hyperacetylated, as confirmed by Co\u2010IP. Atp5f1c K55\u2010Ac decreased ATP enzyme activity and synthesis. Atp5f1c K55 acetylation induced cardiomyocyte senescence, and Sirt4 and Sirt5 regulated Atp5f1c K55 deacetylation. <jats:italic>Conclusion.<\/jats:italic> Our findings reveal a mechanism of RIHD through which Atp5f1c K55\u2010Ac leads to cardiac aging and Sirt4 or Sirt5 modulates Atp5f1c acetylation. Therefore, the regulation of Atp5f1c K55\u2010Ac might be a potential target for the treatment of RIHD.<\/jats:p>","DOI":"10.1155\/2022\/4155565","type":"journal-article","created":{"date-parts":[[2022,9,15]],"date-time":"2022-09-15T21:50:09Z","timestamp":1663278609000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Acetylation of Atp5f1c Mediates Cardiomyocyte Senescence via Metabolic Dysfunction in Radiation\u2010Induced Heart 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