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Open AccessJournal ArticleDOI

Renal ischemia/reperfusion injury; from pathophysiology to treatment.

TLDR
This review summarizes some important potential mechanisms and therapeutic approaches in renal IRI and discusses the design of more targeted therapies to prevent and treatment the injury.
Abstract
Ischemia/reperfusion injury (IRI) is caused by a sudden temporary impairment of the blood flow to the particular organ. IRI usually is associated with a robust inflammatory and oxidative stress response to hypoxia and reperfusion which disturbs the organ function. Renal IR induced acute kidney injury (AKI) contributes to high morbidity and mortality rate in a wide range of injuries. Although the pathophysiology of IRI is not completely understood, several important mechanisms resulting in kidney failure have been mentioned. In ischemic kidney and subsequent of re-oxygenation, generation of reactive oxygen species (ROS) at reperfusion phase initiates a cascade of deleterious cellular responses leading to inflammation, cell death, and acute kidney failure. Better understanding of the cellular pathophysiological mechanisms underlying kidney injury will hopefully result in the design of more targeted therapies to prevent and treatment the injury. In this review, we summarize some important potential mechanisms and therapeutic approaches in renal IRI.

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Journal ArticleDOI

Reperfusion injury and reactive oxygen species: The evolution of a concept.

TL;DR: The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source to activate and enhance ROS production by a second source.
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Measurement and Clinical Significance of Biomarkers of Oxidative Stress in Humans

TL;DR: The clinical significance of biomarkers of oxidative stress in humans must come from a critical analysis of the markers that should give an overall index of redox status in particular conditions.
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Ischemia/Reperfusion Injury Revisited: An Overview of the Latest Pharmacological Strategies.

TL;DR: This review describes many of the latest pharmacological approaches that have been proven effective against IRI, while also revisiting well-established concepts and presenting recent pathophysiological findings in this ever-expanding field.
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Mesenchymal stem cell-derived extracellular vesicles for kidney repair: current status and looming challenges

TL;DR: Current knowledge of MSC-derived EV therapy in experimental AKI and CKD is summarized, and the challenges that need to be addressed are discussed in order to consider M SC-derived EVs as a realistic clinical tool to treat patients with these conditions.
Journal ArticleDOI

HIF-1α-BNIP3-mediated mitophagy in tubular cells protects against renal ischemia/reperfusion injury.

TL;DR: It is demonstrated that HIF-1α-BNIP3-mediated mitophagy in tubular cells plays a protective role through inhibition of apoptosis and ROS production in acute kidney damage.
References
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Journal ArticleDOI

Regulation of cell death: the calcium-apoptosis link.

TL;DR: The dual role of Ca2+ in living organisms is discussed in this paper, where it has been shown that cellular Ca 2+ overload, or perturbation of intracellular Ca2 + compartmentalization, can cause cytotoxicity and trigger either apoptotic or necrotic cell death.
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Acute kidney injury.

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Free radicals as mediators of tissue injury and disease.

TL;DR: This review discusses cellular sources of various radical species and their reactions with vital cellular constituents to provide insights into the controversy over whether free radicals are important mediators of tissue injury.
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RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis.

TL;DR: In this general intensive care unit population, acute kidney 'risk, injury, failure', as defined by the newly developed RIFLE classification, is associated with increased hospital mortality and resource use.
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