Mitochondria as therapeutic targets in acute kidney injury.
- 2016-05-12
Published in:
- Current opinion in nephrology and hypertension. - 2016
Acute Kidney Injury
Antioxidants
Autophagy
Cell Death
Humans
Kidney
Kidney Tubules
Mitochondria
Mitochondrial Dynamics
Mitophagy
Molecular Targeted Therapy
Organelle Biogenesis
Oxidative Stress
English
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.
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.
- Language
-
- English
- Open access status
- green
- Identifiers
-
- DOI 10.1097/MNH.0000000000000228
- PMID 27166518
- Persistent URL
- https://folia.unifr.ch/global/documents/161302
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