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Mitochondria as therapeutic targets in acute kidney injury


Hall, Andrew M; Schuh, Claus-Dieter (2016). Mitochondria as therapeutic targets in acute kidney injury. Current Opinion in Nephrology and Hypertension, 25(4):355-362.

Abstract

PURPOSE OF REVIEW:
Mitochondria are complex intracellular organelles with a variety of important functions. The kidney tubule is densely packed with mitochondria, and mitochondrial dysfunction is thought to be central to the pathogenesis of acute kidney injury (AKI). Mitochondria therefore represent potential targets for novel therapeutic interventions in AKI.
RECENT FINDINGS:
Several mitochondrial targeted approaches have shown promise in recent preclinical studies of AKI, including measures to: reduce oxidative stress within mitochondria; prevent mitochondrial fission and activation of cell death pathways; enhance recycling of damaged mitochondria via autophagy and mitophagy; and accelerate mitochondrial biogenesis postinsult.
SUMMARY:
Recent studies show that it is now eminently feasible to pharmacologically manipulate various key aspects of mitochondrial biology in the kidney, and this has much potential for the future treatment of AKI. However, significant hurdles will have to be overcome in the translational pathway for these strategies to successfully migrate to the clinic.

Abstract

PURPOSE OF REVIEW:
Mitochondria are complex intracellular organelles with a variety of important functions. The kidney tubule is densely packed with mitochondria, and mitochondrial dysfunction is thought to be central to the pathogenesis of acute kidney injury (AKI). Mitochondria therefore represent potential targets for novel therapeutic interventions in AKI.
RECENT FINDINGS:
Several mitochondrial targeted approaches have shown promise in recent preclinical studies of AKI, including measures to: reduce oxidative stress within mitochondria; prevent mitochondrial fission and activation of cell death pathways; enhance recycling of damaged mitochondria via autophagy and mitophagy; and accelerate mitochondrial biogenesis postinsult.
SUMMARY:
Recent studies show that it is now eminently feasible to pharmacologically manipulate various key aspects of mitochondrial biology in the kidney, and this has much potential for the future treatment of AKI. However, significant hurdles will have to be overcome in the translational pathway for these strategies to successfully migrate to the clinic.

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Additional indexing

Item Type:Journal Article, refereed, further contribution
Communities & Collections:04 Faculty of Medicine > Institute of Anatomy
04 Faculty of Medicine > Center for Integrative Human Physiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Scopus Subject Areas:Health Sciences > Internal Medicine
Health Sciences > Nephrology
Language:English
Date:July 2016
Deposited On:25 Jul 2016 09:35
Last Modified:26 Jan 2022 09:43
Publisher:Lippincott Williams & Wilkins
ISSN:1062-4821
OA Status:Green
Publisher DOI:https://doi.org/10.1097/MNH.0000000000000228
PubMed ID:27166518
  • Content: Published Version