PINK1-PRKN/PARK2 pathway of mitophagy is activated to protect against renal ischemia-reperfusion injury
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Summary
It is shown thatmitophagy is induced in renal proximal tubular cells in both in vitro and in vivo models of ischemic AKI, indicating that PINK1-PARK2-mediated mitophagy plays an important role in mitochondrial quality control, tubular cell survival, and renal function during AKI.
- Type
- article
- Published
- 2018-02-17
- Cited by
- 284
- References
- 66
- Access
- Open access
- OpenAlex
- https://openalex.org/W2769676193
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:3374985
Keywords
Mitophagy, Autophagy, PINK1, Mitochondrion, Cell biology
References
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- Mitochondrial Dysregulation and Protection in Cisplatin Nephrotoxicity
Cited by
- Nephrotoxicity and Renal Pathophysiology: A Contemporary Perspective
- Histone deacetylase inhibitors protect against cisplatin-induced acute kidney injury by activating autophagy in proximal tubular cells
- mROS-TXNIP axis activates NLRP3 inflammasome to mediate renal injury during ischemic AKI.
- Mitophagy Plays a Protective Role in Iodinated Contrast-Induced Acute Renal Tubular Epithelial Cells Injury
- Renal ischemia/reperfusion‐induced mitophagy protects against renal dysfunction via Drp1‐dependent‐pathway
- Comparison of iohexol and iodixanol induced nephrotoxicity, mitochondrial damage and mitophagy in a new contrast-induced acute kidney injury rat model
- Endoplasmic Reticulum Stress in Ischemic and Nephrotoxic Acute Kidney Injury
- Aging aggravates hepatic ischemia-reperfusion injury in mice by impairing mitophagy with the involvement of the EIF2α-parkin pathway
- P53 in kidney injury and repair: Mechanism and therapeutic potentials
- Endoplasmic reticulum stress is activated in post-ischemic kidneys to promote chronic kidney disease
- PINK1/Parkin-mediated mitophagy is activated in cisplatin nephrotoxicity to protect against kidney injury
- RNA interference may suppress stress granule formation by preventing argonaute 2 recruitment.
- UCP2‐dependent improvement of mitochondrial dynamics protects against acute kidney injury
- Prohibitin 2-mediated mitophagy attenuates renal tubular epithelial cells injury by regulating mitochondrial dysfunction and NLRP3 inflammasome activation.
- Polydatin mediates Parkin-dependent mitophagy and protects against mitochondria-dependent apoptosis in acute respiratory distress syndrome
- Aged kidneys are refractory to autophagy activation in a rat model of renal ischemia-reperfusion injury
- Nicotinamide reduces renal interstitial fibrosis by suppressing tubular injury and inflammation
- Clearance of damaged mitochondria via mitophagy is important to the protective effect of ischemic preconditioning in kidneys
- Contrast Induced Acute Kidney Injury and Direct Cytotoxicity of Iodinated Radiocontrast Media on Renal Proximal Tubule Cells
- Protective effect and mechanisms of exogenous neutrophil gelatinase-associated lipocalin on lipopolysaccharide-induced injury of renal tubular epithelial cell.
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