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Autophagy protects mitochondrial health in heart failure

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Abstract

The progression of heart failure is reported to be strongly associated with homeostatic imbalance, such as mitochondrial dysfunction and abnormal autophagy, in the cardiomyocytes. Mitochondrial dysfunction triggers autophagic and cardiac dysfunction. In turn, abnormal autophagy impairs mitochondrial function and leads to apoptosis or autophagic cell death under certain circumstances. These events often occur concomitantly, forming a vicious cycle that exacerbates heart failure. However, the role of the crosstalk between mitochondrial dysfunction and abnormal autophagy in the development of heart failure remains obscure and the underlying mechanisms are mainly elusive. The potential role of the link between mitochondrial dysfunction and abnormal autophagy in heart failure progression has recently garnered attention. This review summarized recent advances of the interactions between mitochondria and autophagy during the development of heart failure.

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Acknowledgements

We would like to show our gratitude to Yifei Ruan, who has checked and revised the content of the manuscript, prepared the response and modified Figure 2, during the revision period.

Funding

This work was supported by grants to Yanmei Chen from the National Natural Science Foundation of China (no. 81970239), GuangDong Basic and Applied Basic Research Foundation (grant 2023A1515010381 and grant 2022A1515220013 to Y.C.) and the Natural Science Foundation of Jiangxi Province (grant 20232ACB216003 to Y.C.).

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Among the authors in the list, Yating Tang wrote the main manuscript text and prepared figures 1-6. Wenlong Xu, Jiajun Zhou and Yu Liu participated in the collection and collation of references. Jiajun Zhou checked the grammar and polished the article. Kai Cui and Yanmei Chen reviewed and revised the manuscript. All authors reviewed the manuscript.

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Tang, Y., Xu, W., Liu, Y. et al. Autophagy protects mitochondrial health in heart failure. Heart Fail Rev 29, 113–123 (2024). https://doi.org/10.1007/s10741-023-10354-x

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