Mechanisms and Functions of Mitophagy and Potential Roles in Renal Disease

Zuo, Zhenying; Jing, Kaipeng; Wu, Huixing; Wang, Shujun; Ye, Lin; Li, Zhihang; Yang, Chen; Pan, Qingjun; Liu, Wei Jing; Liu, Huafeng

doi:10.3389/fphys.2020.00935

Cited by 38 publications

(48 citation statements)

References 154 publications

(231 reference statements)

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“…Thus, PINK1 accumulates at the mitochondrial outer membrane, where it recruits Parkin (an E3 ubiquitin ligase) from the cytoplasm to the surface of the mitochondria ( Xu et al, 2020 ). PINK1 phosphorylates and activates Parkin, which can then ubiquitinate mitochondrial membrane proteins ( Capasso et al, 2020 ; Villacampa et al, 2020 ; Zuo et al, 2020 ). This ubiquitination allows mitochondria to be recognized and swallowed by autophagic vesicles and wrapped in a double-layer membrane structure.…”

Section: Receptor-dependent and Receptor-independent Pathwaysmentioning

confidence: 99%

RETRACTED: Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets

Kimberlee

et al. 2021

Front. Physiol.

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A variety of complex risk factors and pathological mechanisms contribute to myocardial stress, which ultimately promotes the development of cardiovascular diseases, including acute cardiac insufficiency, myocardial ischemia, myocardial infarction, high-glycemic myocardial injury, and acute alcoholic cardiotoxicity. Myocardial stress is characterized by abnormal metabolism, excessive reactive oxygen species production, an insufficient energy supply, endoplasmic reticulum stress, mitochondrial damage, and apoptosis. Mitochondria, the main organelles contributing to the energy supply of cardiomyocytes, are key determinants of cell survival and death. Mitophagy is important for cardiomyocyte function and metabolism because it removes damaged and aged mitochondria in a timely manner, thereby maintaining the proper number of normal mitochondria. In this review, we first introduce the general characteristics and regulatory mechanisms of mitophagy. We then describe the three classic mitophagy regulatory pathways and their involvement in myocardial stress. Finally, we discuss the two completely opposite effects of mitophagy on the fate of cardiomyocytes. Our summary of the molecular pathways underlying mitophagy in myocardial stress may provide therapeutic targets for myocardial protection interventions.

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Section: Receptor-dependent and Receptor-independent Pathwaysmentioning

confidence: 99%

RETRACTED: Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets

Kimberlee

et al. 2021

Front. Physiol.

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“…Mitophagy is a mechanism by which damaged mitochondria are eliminated within a cell after stress challenges. 186,187 It is regulated by, among others, PINK1 (PTEN-induced putative kinase 1) 28,188 and autophagy proteins microtubule-associated protein 1A/1B-light chain 3I (LC-3I) and p62 in proximal tubules. 188,189 Using rat as an FA-AKI model, Aparicio-Trejo et al 155 demonstrated that PINK1 and p62…”

Section: Impaired Mitophagymentioning

confidence: 99%

Folic acid‐induced animal model of kidney disease

2021

Anim Models and Exp Med

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Kidney disease may be generally classified clinically into two categories: acute kidney injury (AKI) and chronic kidney disease (CKD), both of which are tightly interconnected. 1-3 AKI can often develop in clinical settings in critically ill patients, leading to increased morbidity and mortality. 4,5 AKI is manifested by a rapid decline in the glomerular filtration rates (GFRs) 6 and its pathogenesis is complex, involving ischemia, sepsis, drug toxicity, and trauma. 7 If left unmanaged, AKI can develop into CKD, which is characterized by a progressive decrease in GFR, culminating in a gradual loss of renal function. 8 The transition from AKI to CKD can also be hastened by numerous risk factors such as obesity, hypertension, diabetes, and chronic inflammation. 9-11 Currently, there are no effective treatments for either AKI or CKD, stressing a continual need to elucidate the underlying pathological mechanisms of AKI and CKD. In this regard, animal models of kidney disease have been invaluable in that utilization of these animal models not only facilitates our understanding of the

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“…This disruption of mitochondrial homeostasis is linked with redox imbalance and oxidative stress accompanied with impairment of mitochondrial membrane potential and release of apoptosis stimulating factors such as cytochrome c and apoptosis inducing factor (AIF) [ 133 , 134 , 135 , 136 ]. These deranged mitochondrial dynamics, if left unattended or uncorrected, would eventually lead to accumulation of damaged mitochondria, which could overwhelm the mitophagy capacity that is regulated by key proteins such as PINK1 and Parkin [ 137 , 138 , 139 , 140 ], resulting in cell death and worsened diabetic kidney injury. Therefore, mitochondrial homeostasis and dynamics can also serve as targets for renal therapy in DKD.…”

Section: Redox Imbalance-linked Mitochondrial Dysfunction In Dkdmentioning

confidence: 99%

NADH/NAD+ Redox Imbalance and Diabetic Kidney Disease

2021

Biomolecules

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Diabetic kidney disease (DKD) is a common and severe complication of diabetes mellitus. If left untreated, DKD can advance to end stage renal disease that requires either dialysis or kidney replacement. While numerous mechanisms underlie the pathogenesis of DKD, oxidative stress driven by NADH/NAD+ redox imbalance and mitochondrial dysfunction have been thought to be the major pathophysiological mechanism of DKD. In this review, the pathways that increase NADH generation and those that decrease NAD+ levels are overviewed. This is followed by discussion of the consequences of NADH/NAD+ redox imbalance including disruption of mitochondrial homeostasis and function. Approaches that can be applied to counteract DKD are then discussed, which include mitochondria-targeted antioxidants and mimetics of superoxide dismutase, caloric restriction, plant/herbal extracts or their isolated compounds. Finally, the review ends by pointing out that future studies are needed to dissect the role of each pathway involved in NADH-NAD+ metabolism so that novel strategies to restore NADH/NAD+ redox balance in the diabetic kidney could be designed to combat DKD.

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Mechanisms and Functions of Mitophagy and Potential Roles in Renal Disease

Cited by 38 publications

References 154 publications

RETRACTED: Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets

RETRACTED: Molecular Perspectives of Mitophagy in Myocardial Stress: Pathophysiology and Therapeutic Targets

Folic acid‐induced animal model of kidney disease

NADH/NAD+ Redox Imbalance and Diabetic Kidney Disease

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