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Wang, Chao-Yung; Chen, Chun-Chi; Lin, Mei-Hsiu; Su, Hui-Ting; Ho, Ming-Yun; Yeh, Jih-Kai; Tsai, Ming-Lung; Hsieh, I-Chang; Wen, Ming-Shien
Biology (Basel, Switzerland), 11/2020, Letnik: 9, Številka: 11Journal Article
Simple Summary: We described the existence of an integrated Beclin 1, TLR9, and SIRT3 network involving autophagy, oxidative stress, and mitochondria that is essential for empagliflozin to protect against doxorubicin toxicity in the heart. Empagliflozin treatment increases the abundance of mitochondrial SIRT3 and enhances the activation of TLR9 to bind with Beclin 1, triggering communication to the autophagic, immune system, and inflammatory machinery. From a therapeutic standpoint, SIRT3 loss-of-function variant DCM patients lose the empagliflozin-protective effects, since SIRT3 is implicated in modern world diseases, such as aging, circadian disturbance, and obesity.
