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Mitochondrial complex I deficiency and cardiovascular diseases: current evidence and future directions

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Abstract

Compelling evidence demonstrates the emerging role of mitochondrial complex I deficiency in the onset and development of cardiovascular diseases (CVDs). In particular, defects in single subunits of mitochondrial complex I have been associated with cardiac hypertrophy, ischemia/reperfusion injury, as well as diabetic complications and stroke in pre-clinical studies. Moreover, data obtained in humans revealed that genes coding for complex I proteins were associated with different CVDs. In this review, we discuss recent experimental studies that underline the contributory role of mitochondrial complex I deficiency in the etiopathogenesis of several CVDs, with a particular focus on those involving loss of function models of mitochondrial complex I. We also discuss human studies and potential therapeutic strategies able to rescue mitochondrial function in CVDs.

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Acknowledgments

This work was supported by grants from the Italian Ministry of Health and the “5 per mille” grant.

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Forte, M., Palmerio, S., Bianchi, F. et al. Mitochondrial complex I deficiency and cardiovascular diseases: current evidence and future directions. J Mol Med 97, 579–591 (2019). https://doi.org/10.1007/s00109-019-01771-3

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