Review Article

Mitophagy, Mitochondrial Dynamics, and Homeostasis in Cardiovascular Aging

Table 1

Alterations in mitochondrial dynamics and turnover for aging and CVD.

ProteinAlterationAge-related disease/phenotypeOrganism/modelReferences

Mfn2Reduced expressionHyperproliferation of vascular smooth muscle cellsRats or mice: hypertensive and atherosclerotic arteries[159]
Accelerated cardiac hypertrophy and cardiomyopathyMouse heart[38, 160, 161]
Mfn1Increased expressionDecreased glycolysis, increased oxygen consumption rate, and ATP levelsOld normal human fibroblasts[162]
Opa1Reduced expressionAccelerated heart failureHeart from humans, rats, and mice[52, 163, 164]
Increased expressionProtection from ischemia-reperfusion (I/R) injuryMouse heart[165]
Decreased glycolysis, increased oxygen consumption rate, and ATP levelsOld normal human fibroblasts[162]
Drp1Reduced expressionDevelopment of cardiac dysfunctionMouse heart[166, 167]
Attenuated diabetes-induced cardiac dysfunctionStreptozotocin- (STZ-) induced diabetic mice[66]
Protection against posttraumatic/diabetes-induced cardiac dysfunctionAdult rats[168]
InhibitionProtection from cardiac hypertrophy and function after I/R injury or myocardial infarctionMouse heart[169, 170]
Improved LV functions, reduced MI sizeMouse heart[64]
Protection from Dox-induced cardiac damageH9c2[65]
Short-term induction in midlifeProlonged lifespanDrosophila melanogaster[62]
PINK1Increased expressionIncreased cell senescenceNeonatal rat cardiomyocytes[125]
ActivationImproved mitochondrial function, decreased ROS production, decreased apoptosisMouse heart[124]
ParkinIncreased expressionProlonged lifespanDrosophila melanogaster[171]
Decayed agingMouse[172]
Reduced expressionImpaired recovery of cardiac contractilityMouse heart[173]
FUNDC1AbrogationSustained mitochondrial fission, cell death, and heart failureAdult mice cardiac progenitor cells (CPCs)[104]
Increased expressionIncreased mitophagy and reduced platelet activity, protection from I/R injuryMouse[125]
Infarction area expansion and cardiac dysfunction following acute cardiac IR injuryMouse[85]
BNIP3Suppressed activityStressed cardiomyocytesHuman heart[174]
BECN1/Beclin1Increased expressionAttenuated heart failureMouse heart[60]
Deceased interaction with BCL-2Improved healthspan, prolonged longevityMutant mice[175]
PCG-1αOverexpressionSuppressed aging-induced mitophagy, improved mitochondriaMouse skeletal muscle[129]