Autophagy in acute kidney injury.
Acute kidney injury is a major kidney disease associated with poor clinical outcomes. The pathogenesis of acute kidney injury is multifactorial and is characterized by tubular cell injury and death. Recent studies have shown autophagy induction in proximal tubular cells during acute kidney injury. The regulatory mechanisms of tubular cell autophagy are poorly understood; however, some recent findings have set up a foundation for further investigation. Although autophagy may promote cell death under certain experimental conditions, pharmacologic and autophagy-related gene knockout studies have established a renoprotective role for autophagy in acute kidney injury. The mechanisms by which autophagy protects cells from injury and how, possibly, its pro-survival role switches to pro-death under certain conditions are discussed. Further research is expected to help us understand the regulatory network of tubular cell autophagy, define its precise roles in the specific context of acute kidney injury, and identify autophagy-targeting strategies for the prevention and treatment of acute kidney injury.
Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; Department of Cellular Biology and Anatomy, Medical College of Georgia at Georgia Regents University and Charlie Norwood VA Medical Center, Augusta, GA.
Man J
MJ
Livingston
Department of Nephrology, The Second Xiangya Hospital, Central South University, Changsha, Hunan 410011, China; Department of Cellular Biology and Anatomy, Medical College of Georgia at Georgia Regents University and Charlie Norwood VA Medical Center, Augusta, GA. Electronic address: zdong@gru.edu.
Zheng
Z
Dong
D058186:Acute Kidney Injury / Q000473:pathology* / Q000628:therapy; D000818:Animals; D001343:Autophagy / Q000502:physiology*; D000071187:Autophagy-Related Protein 5; D000071189:Autophagy-Related Protein-1 Homolog; D006801:Humans; D051795:Hypoxia-Inducible Factor 1, alpha Subunit / Q000502:physiology; D047908:Intracellular Signaling Peptides and Proteins / Q000502:physiology; D007687:Kidney Tubules, Proximal / Q000473:pathology; D008565:Membrane Proteins / Q000502:physiology; D008869:Microtubule-Associated Proteins / Q000502:physiology; D018384:Oxidative Stress; D017346:Protein Serine-Threonine Kinases / Q000502:physiology; D011518:Proto-Oncogene Proteins / Q000502:physiology; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
C502778:ATG5 protein, human; D000071187:Autophagy-Related Protein 5; C090121:BNIP3 protein, human; D051795:Hypoxia-Inducible Factor 1, alpha Subunit; D047908:Intracellular Signaling Peptides and Proteins; D008565:Membrane Proteins; D008869:Microtubule-Associated Proteins; D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D000071189:Autophagy-Related Protein-1 Homolog; D017346:Protein Serine-Threonine Kinases; C484754:ULK1 protein, human
Acute kidney injury; autophagy; cell death; cell survival