Renal Ischemia-Reperfusion Injury Molecular Mechanisms and Therapeutic Targets | ||
| Minia Journal of Medical Research | ||
| Volume 32, Issue 2, April 2021, Pages 42-49 PDF (370.88 K) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/mjmr.2021.231544 | ||
| Authors | ||
| Sherief A. Maher1; Michael A. Fawzy2; Mahmoud A. El-Rehany1; Moustafa Fathy3 | ||
| 1Department of Biochemistry, Faculty of Pharmacy, Deraya University, Minia, Egypt | ||
| 2Department of Biochemistry, Faculty of Pharmacy, Minia University, Minia, Egypt | ||
| 3Department 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. | ||
| Keywords | ||
| Ischemia/reperfusion injury; reactive oxygen species; oxidative stress response; hypoxia | ||
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