{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,12]],"date-time":"2026-01-12T10:30:48Z","timestamp":1768213848514,"version":"3.49.0"},"reference-count":40,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2025,12,19]],"date-time":"2025-12-19T00:00:00Z","timestamp":1766102400000},"content-version":"vor","delay-in-days":18,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,12,1]],"date-time":"2025-12-01T00:00:00Z","timestamp":1764547200000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Medicine"],"published-print":{"date-parts":[[2025,12]]},"abstract":"ABSTRACT<\/jats:title>\n \n Objectives<\/jats:title>\n \n To explore the mechanism of\n RNA<\/jats:styled-content>\n oxidation and its inhibitor\n MTHI<\/jats:styled-content>\n involved in cardiomyocyte hypertrophy.\n <\/jats:p>\n <\/jats:sec>\n \n Methods<\/jats:title>\n \n The hypertrophic H9c2 cardiomyocytes were stimulated with different concentrations and times of Ang\n II<\/jats:styled-content>\n (Ang\n II<\/jats:styled-content>\n ) to construct a model of hypertensive heart failure in\u00a0vitro. Transfection of H9c2 cells with the\n MTH1<\/jats:styled-content>\n overexpression plasmid was performed. The\n mRNA<\/jats:styled-content>\n expression of\n ANP<\/jats:styled-content>\n ,\n BNP<\/jats:styled-content>\n , and \u03b2\u2010MHC in each experimental group was detected by\n PCR<\/jats:styled-content>\n . The expression of 8\u2010\n oxoG<\/jats:styled-content>\n in H9c2 cells was determined by immunofluorescence and enzyme\u2010linked immunosorbent assay (\n ELISA<\/jats:styled-content>\n ). The activation of the\n ERK<\/jats:styled-content>\n \u2013\n MAPK<\/jats:styled-content>\n pathway and the amount of\n MTH1<\/jats:styled-content>\n protein were detected by\n WB<\/jats:styled-content>\n semi\u2010quantitative method.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n Notably,\n RNA<\/jats:styled-content>\n oxidation is a critical event in cellular senescence, and its accumulation is strongly linked to the aging process and the development of age\u2010related diseases. In our model of cardiomyocyte hypertrophy, the oxidative damage of\n RNA<\/jats:styled-content>\n was aggravated, and the expression of\n MTH1<\/jats:styled-content>\n was increased. At the same time, the sequence of\n ERK<\/jats:styled-content>\n \u2013\n MAPK<\/jats:styled-content>\n pathway proteins was activated. It can be seen that the oxidative damage of\n RNA<\/jats:styled-content>\n is related to the process of cardiomyocyte hypertrophy. After transfection of the\n MTH1<\/jats:styled-content>\n overexpression plasmid into the cardiomyocyte hypertrophy model, we found that the amount of 8\u2010\n oxoG<\/jats:styled-content>\n decreased, and the activation of\n ERK<\/jats:styled-content>\n \u2013\n MAPK<\/jats:styled-content>\n signaling pathway proteins decreased, and H9c2 cell hypertrophy decreased. Therefore, we concluded that 8\u2010\n oxoG<\/jats:styled-content>\n may aggravate the hypertrophy of the cardiomyocyte hypertrophy model by activating the\n ERK<\/jats:styled-content>\n \u2013\n MAPK<\/jats:styled-content>\n pathway.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusion<\/jats:title>\n \n The oxidative damage of\n RNA<\/jats:styled-content>\n is involved in the process of cardiomyocyte hypertrophy. The mechanism may be that 8\u2010\n oxoG<\/jats:styled-content>\n , a product of\n RNA<\/jats:styled-content>\n oxidation, activates the downstream\n ERK<\/jats:styled-content>\n \u2013\n MAPK<\/jats:styled-content>\n signaling pathway. These findings provide new perspectives for further exploration into the role of\n RNA<\/jats:styled-content>\n oxidation in the pathogenesis of age\u2010related diseases, particularly heart failure.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1002\/agm2.70057","type":"journal-article","created":{"date-parts":[[2025,12,20]],"date-time":"2025-12-20T04:20:52Z","timestamp":1766204452000},"page":"612-623","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Mechanism of\n RNA<\/scp>\n Oxidation and Its Inhibitor Involved in\n Ang II<\/scp>\n \u2010Induced Cardiomyocyte Hypertrophy"],"prefix":"10.1002","volume":"8","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-6214-7225","authenticated-orcid":false,"given":"Tong","family":"Liu","sequence":"first","affiliation":[{"name":"Department of Cardiology Beijing Anzhen Hospital, Capital Medical University Beijing 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