Protective Mitophagy in Human Hypoxic Cardiomyocytes: Mechanistic Insights into SGLT2 Inhibitor Dapagliflozin Cardioprotection in Ischemic Injury

    April 2026 in “ Research Square ”
    Y.‐H. Lin, Shih-Jie Jhuo, Wei-Chung Tsai, Yi‐Hsueh Liu, Nai-Yu Chi, T Y Huang, Wei-Tsung Wu, Tsung-Hsien Lin, Wen-Ter Lai, Sheng‐Hsiung Sheu, Chun-Yuan Chu, Po‐Chao Hsu
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    TLDR Dapagliflozin helps protect heart cells under stress by improving mitochondrial function and reducing cell damage.
    This study examines the cardioprotective effects of the SGLT2 inhibitor dapagliflozin on human cardiomyocytes derived from induced pluripotent stem cells under hypoxic stress. Dapagliflozin was found to reverse hypoxia-induced gene expression changes, affecting thousands of genes, and activate the AMPK/SIRT1/SIRT3 signaling pathway. This activation enhances autophagy and mitophagy, leading to improved mitochondrial function, reduced apoptosis, and restored mitochondrial membrane potential. The study highlights dapagliflozin's potential therapeutic role in myocardial ischemic injury by promoting mitochondrial quality control and adaptive autophagy, thereby enhancing cell survival and reducing myocardial injury.
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