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Mitochondrial Dysfunction and Mitophagy: Physiological Implications in Cardiovascular Health

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Biochemistry of Apoptosis and Autophagy

Part of the book series: Advances in Biochemistry in Health and Disease ((ABHD,volume 18))

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Abstract

Heart failure is the typical end stage for cardiovascular diseases and presents a major public health burden. Heart failure occurs as a result of an excess loss of cardiac myocytes and increased fibrosis, which leads to a reduced capacity to sustain contractile function. Cardiac myocytes are highly enriched in mitochondria which are responsible for generating energy via oxidative phosphorylation. Although mitochondria are critical for myocyte function, they can become harmful when damaged or dysfunctional. Therefore, the quality of mitochondria must be carefully and continuously monitored to ensure cellular homeostasis. Mitochondrial autophagy or mitophagy refers to the selective engulfment of mitochondria by autophagosomes. This selective elimination of mitochondria in response to various bioenergetic or environmental cues is responsible for regulating both mitochondrial quality and quantity and is critical for maintaining a healthy population of mitochondria. Defects in this process affect cardiac homeostasis and contribute to cardiac aging and development of various myocardial pathologies. This chapter provides insights into the molecular mechanisms involved in regulating mitophagy in cells and examines the functional importance of mitophagy in the myocardium.

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Acknowledgements

Å.B. Gustafsson is supported by grants from NIH (R01HL138560 and R01HL132300), and TRDRP (27IR-0013 and 28IP-0025).

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Gustafsson, Å.B. (2022). Mitochondrial Dysfunction and Mitophagy: Physiological Implications in Cardiovascular Health. In: Kirshenbaum, L.A. (eds) Biochemistry of Apoptosis and Autophagy. Advances in Biochemistry in Health and Disease, vol 18. Springer, Cham. https://doi.org/10.1007/978-3-030-78799-8_11

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