Mitochondrial dynamics: Orchestrating the journey to advanced age.
Aging is a degenerative process that unfortunately is an inevitable part of life and risk factor for cardiovascular disease including heart failure. Among the several theories purported to explain the effects of age on cardiac dysfunction, the mitochondrion has emerged a central regulator of this process. Hence, it is not surprising that abnormalities in mitochondrial quality control including biogenesis and turnover have such detrimental effects on cardiac function. In fact mitochondria serve as a conduit for biological signals for apoptosis, necrosis and autophagy respectively. The removal of damaged mitochondria by autophagy/mitophagy is essential for mitochondrial quality control and cardiac homeostasis. Defects in mitochondrial dynamism fission/fusion events have been linked to cardiac senescence and heart failure. In this review we discuss the impact of aging on mitochondrial dynamics and senescence on cardiovascular health. This article is part of a Special Issue entitled: CV Aging.
The Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba R2H 2A6, Canada; Department of Physiology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada; Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada.
Agnieszka K
AK
Biala
The Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba R2H 2A6, Canada; Department of Physiology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada; Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada.
Rimpy
R
Dhingra
The Institute of Cardiovascular Sciences, St. Boniface Hospital Research Centre, Winnipeg, Manitoba R2H 2A6, Canada; Department of Physiology, Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada; Faculty of Health Sciences, College of Medicine, University of Manitoba, Winnipeg, Manitoba R2H 2A6, Canada. Electronic address: Lorrie@sbrc.ca.
Lorrie A
LA
Kirshenbaum
D000375:Aging / Q000378:metabolism* / Q000473:pathology; D000818:Animals; D031204:Caloric Restriction; D016923:Cell Death; D005786:Gene Expression Regulation; D006333:Heart Failure / Q000235:genetics / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D008928:Mitochondria / Q000378:metabolism* / Q000473:pathology; D063154:Mitochondrial Dynamics / Q000235:genetics*; D024101:Mitochondrial Proteins / Q000235:genetics / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism* / Q000473:pathology; D018384:Oxidative Stress; D015398:Signal Transduction; D037761:Sirtuins / Q000235:genetics / Q000378:metabolism
D024101:Mitochondrial Proteins; D037761:Sirtuins
Aging; Cell death; Mitochondrial dynamics; Oxidative stress; ROS