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Non-coding RNAs regulating mitochondrial function in cardiovascular diseases

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Abstract

Cardiovascular disease (CVD) is the leading cause of disease-related death worldwide and a significant obstacle to improving patients’ health and lives. Mitochondria are core organelles for the maintenance of myocardial tissue homeostasis, and their impairment and dysfunction are considered major contributors to the pathogenesis of various CVDs, such as hypertension, myocardial infarction, and heart failure. However, the exact roles of mitochondrial dysfunction involved in CVD pathogenesis remain not fully understood. Non-coding RNAs (ncRNAs), particularly microRNAs, long non-coding RNAs, and circular RNAs, have been shown to be crucial regulators in the initiation and development of CVDs. They can participate in CVD progression by impacting mitochondria and regulating mitochondrial function-related genes and signaling pathways. Some ncRNAs also exhibit great potential as diagnostic and/or prognostic biomarkers as well as therapeutic targets for CVD patients. In this review, we mainly focus on the underlying mechanisms of ncRNAs involved in the regulation of mitochondrial functions and their role in CVD progression. We also highlight their clinical implications as biomarkers for diagnosis and prognosis in CVD treatment. The information reviewed herein could be extremely beneficial to the development of ncRNA-based therapeutic strategies for CVD patients.

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This work was supported by the China Postdoctoral Science Foundation (2018M642607).

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Xiang Ao: original draft preparation, funding acquisition. Wei Ding: review and editing, data curation. Xiaoge Li: data curation. Qingling Xu: data curation. Xinhui Chen: data curation. Xuehao Zhou: data curation. Jianxun Wang: review and editing. Ying Liu: writing—conceptualization, original draft preparation, writing—review and editing.

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Ao, X., Ding, W., Li, X. et al. Non-coding RNAs regulating mitochondrial function in cardiovascular diseases. J Mol Med 101, 501–526 (2023). https://doi.org/10.1007/s00109-023-02305-8

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  • DOI: https://doi.org/10.1007/s00109-023-02305-8

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