Browsing by Author "Guo, Rui"

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    Editorial: Role of Mitochondrial Quality Control in Myocardial and Microvascular Physiology and Pathophysiology
    (Frontiers Media S.A, 2021-09) Lochner, Amanda; Wang, Hsueh-Hsiao; Reiter, Russel J.; Guo, Rui; Zhou, Hao
    Mitochondrial quality control (MQC) involves a series of adaptive responses of mitochondrial morphological alterations and functional modifications, such as mitochondrial fusion, mitochondrial fission, mitophagy, mitochondrial biogenesis, mitochondrial bioenergetics, and mitochondria-mediated death pathways (Akbari et al., 2019; Del Campo, 2019; Shanmughapriya et al., 2020; Wang et al., 2020c). Mitochondrial damage or impaired MQC has been reported to play an important role in regulating the physiology and/or pathology of myocardium and vessels (Heusch, 2019; Hughes et al., 2020; Wang and Zhou, 2020; Wang et al., 2020b). The objective role of the Research Topic “Role of Mitochondrial Quality Control in Myocardial and Microvascular Physiology and Pathophysiology” (https://www.frontiersin.org/research-topics/13532/role-of-mitochondrial-quality-control-in-myocardial-and-microvascular-physiology-and-pathophysiology#research-topic-overview) was to gather original research articles and/or reviews to highlight the recent findings regarding the impact of MQC on various cardiovascular disorders. The article “Physical exercise: a novel tool to protect mitochondrial health” by Sorriento et al. reviews the effects of physical activity on cardiac mitochondrial function underlying the ability to modulate specific steps in mitochondrial quality control in both physiological and pathophysiological conditions. Topics were discussed ranged from the effects of exercise on mitochondrial phenotypes, biogenesis, turnover, morphology and respiration to cardiac pathophysiological conditions such as, aging, ischemia/reperfusion injury (I/R), diabetic cardiomyopathy, and anthracyclines dependent heart failure. From these studies, physical exercise emerges as a non-pharmacological tool (“mitochondrial medicine for muscle”) to improve cardiovascular fitness in healthy people as well as to attenuate mitochondrial dysfunction in patients with pathophysiological conditions, particularly cardiac I/R damage.