Renal Ischemia-Reperfusion Injury Molecular Mechanisms and Therapeutic Targets

Document Type : Original Article

Authors

1 Department of Biochemistry, Faculty of Pharmacy, Deraya University, Minia, Egypt

2 Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia, Egypt

3 Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia, Egypt University, University of Toyama, Toyama, Japan

Abstract

Ischemia/reperfusion injury (IRI) is caused by a rapid transient reduction in blood flow to a specific 
organ. IRI is typically accompanied by a strong inflammatory and oxidative stress response to 
hypoxia and reperfusion, which disrupts organ function. AKI caused by renal IRI contributes to a high 
morbidity and death rate in a variety of injuries. Although the pathophysiology of IRI is not fully 
understood, numerous key pathways leading to renal failure have been identified. The production of 
reactive oxygen species (ROS) during the reperfusion phase of the ischemic kidney and subsequent 
re-oxygenation begins a cascade of detrimental cellular reactions that lead to inflammation, cell 
death, and acute kidney failure. Greater knowledge of the cellular pathophysiological mechanisms 
causing kidney damage may lead to the development of more focused treatments to prevent and treat 
the damage. We discuss several significant possible mechanisms and treatment methods in renal IRI 
in this study.

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