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Published in: Inflammopharmacology 4/2023

02-05-2023 | Acute Kidney Injury | Review

Ischemic tubular injury: Oxygen-sensitive signals and metabolic reprogramming

Authors: Yalda Rahbar Saadat, Seyed Mahdi Hosseiniyan Khatibi, Anis Sani, Sepideh Zununi Vahed, Mohammadreza Ardalan

Published in: Inflammopharmacology | Issue 4/2023

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Abstract

The kidneys are the most vulnerable organs to severe ischemic insult that results in cellular hypoxia under pathophysiological conditions. Large amounts of oxygen are consumed by the kidneys, mainly to produce energy for tubular reabsorption. Beyond high oxygen demand and the low oxygen supply, different other factors make kidneys vulnerable to ischemia which is deemed to be a major cause of acute kidney injury (AKI). On the other hand, kidneys are capable of sensing and responding to oxygen alternations to evade harms resulting from inadequate oxygen. The hypoxia-inducible factor (HIF) is the main conserved oxygen-sensing mechanism that maintains homeostasis under hypoxia through direct/indirect regulation of several genes that contribute to metabolic adaptation, angiogenesis, energy conservation, erythropoiesis, and so on. In response to oxygen availability, prolyl-hydroxylases (PHDs) control the HIF stability. This review focuses on the oxygen-sensing mechanisms in kidneys, particularly in proximal tubular cells (PTCs) and discusses the molecules involved in ischemic response and metabolic reprogramming. Moreover, the possible roles of non-coding RNAs (microRNAs and long non-coding RNAs) in the development of ischemic AKI are put forward.
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Metadata
Title
Ischemic tubular injury: Oxygen-sensitive signals and metabolic reprogramming
Authors
Yalda Rahbar Saadat
Seyed Mahdi Hosseiniyan Khatibi
Anis Sani
Sepideh Zununi Vahed
Mohammadreza Ardalan
Publication date
02-05-2023
Publisher
Springer International Publishing
Published in
Inflammopharmacology / Issue 4/2023
Print ISSN: 0925-4692
Electronic ISSN: 1568-5608
DOI
https://doi.org/10.1007/s10787-023-01232-x

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