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Int. J. Mol. Sci. 2016, 17(5), 662;

Autophagy, Innate Immunity and Tissue Repair in Acute Kidney Injury

Department of Internal Medicine—Cardiovascular Medicine, the Ohio State University, Columbus, OH 43210, USA
Davis Heart and Lung Research Institute, the Ohio State University, Columbus, OH 43210, USA
1st Department of Critical Care Medicine & Pulmonary Services, Evangelismos Hospital, National and Kapodistrian University of Athens School of Medicine, GP Livanos and M. Simou Laboratories, Athens 10675, Greece
Robert Wood Johnson Medical School, Rutgers Biomedical and Health Sciences, New Brunswick, NJ 08903-0019, USA
Department of Surgery, the Ohio State University, Columbus, OH 43210, USA
Authors to whom correspondence should be addressed.
Academic Editor: Alan Parrish
Received: 17 March 2016 / Revised: 14 April 2016 / Accepted: 20 April 2016 / Published: 3 May 2016
(This article belongs to the Special Issue Advances in Chronic Kidney Disease)
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Kidney is a vital organ with high energy demands to actively maintain plasma hemodynamics, electrolytes and water homeostasis. Among the nephron segments, the renal tubular epithelium is endowed with high mitochondria density for their function in active transport. Acute kidney injury (AKI) is an important clinical syndrome and a global public health issue with high mortality rate and socioeconomic burden due to lack of effective therapy. AKI results in acute cell death and necrosis of renal tubule epithelial cells accompanied with leakage of tubular fluid and inflammation. The inflammatory immune response triggered by the tubular cell death, mitochondrial damage, associative oxidative stress, and the release of many tissue damage factors have been identified as key elements driving the pathophysiology of AKI. Autophagy, the cellular mechanism that removes damaged organelles via lysosome-mediated degradation, had been proposed to be renoprotective. An in-depth understanding of the intricate interplay between autophagy and innate immune response, and their roles in AKI pathology could lead to novel therapies in AKI. This review addresses the current pathophysiology of AKI in aspects of mitochondrial dysfunction, innate immunity, and molecular mechanisms of autophagy. Recent advances in renal tissue regeneration and potential therapeutic interventions are also discussed. View Full-Text
Keywords: ischemia-reperfusion injury; nephrotoxicity; oxidative stress; kidney disease; tissue regeneration ischemia-reperfusion injury; nephrotoxicity; oxidative stress; kidney disease; tissue regeneration

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Duann, P.; Lianos, E.A.; Ma, J.; Lin, P.-H. Autophagy, Innate Immunity and Tissue Repair in Acute Kidney Injury. Int. J. Mol. Sci. 2016, 17, 662.

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