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Increased oxidative stress, persistent inflammation, mitochondrial dysfunction, and cellular senescence represent common age-associated mechanisms that amplify disease progression and severity, underscoring the necessity for targeted therapeutic approaches

Acknowledgements This research was supported by the National Key R&D Program of China (2024YFA1212500), the National Natural Science Foundation of China projects (32171320 and 82302384), the Key Project of the Natural Science Foundation of Shaanxi Province (2025JC-QYCX-066), the National University of Singapore (NUHSRO/2020/133/Startup/08, NUHSRO/2023/008/NUSMed/TCE/LOA, NUHSRO/2021/034/TRP/09/Nanomedicine, 23-0173-A0001), the National Medical Research Council (MOH-001388-00, CG21APR1005, OFIRG23jul-0047), the National Research Foundation (NRF-000352-00), and start-up funding from Shandong Cancer Hospital (rcyj-202603) Ethics declarations Competing interests The authors declare no competing interests

This redox imbalance triggers lipid peroxidation (e.g., elevated malondialdehyde MDA), protein carbonylation (e.g., 3-nitrotyrosine accumulation), and mitochondrial DNA oxidative damage (e.g., increased 8-hydroxy-2-deoxyguanosine 8-OHdG) via Fenton reactions, ultimately promoting cardiomyocyte apoptosis and contractile dysfunction (Tsutsui et al., 2011)

The resulting images were processed by LAS X imaging software (Leica Microsystems, Germany) and ImageJ (Schneider et al., 2012)

REST, RE1-silencing transcription factor