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Targeting ferroptosis in ischemia/reperfusion renal injury

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Abstract

Renal I/R injury is a severe medical condition contributing to acute kidney injury (AKI), leading to rapid kidney dysfunction and high mortality rates. It is generally observed during renal transplantation, shock, trauma, and urologic and cardiovascular surgery, for which there is no effective treatment. Cell death and damage are commonly linked to I/R. Cell death triggered by iron-dependent lipid peroxidation, such as ferroptosis, has been demonstrated to have a significant detrimental effect in renal IRI models, making it a new type of cell death currently being researched. Ferroptosis is a nonapoptotic type of cell death that occurs when free iron enters the cell and is a critical component of many biological processes. In ferroptosis-induced renal I/R injury, iron chelators such as Deferasirox, Deferiprone, and lipophilic antioxidants are currently suppressed lipid peroxidation Liproxstatin-1 (Lip-1), Ferrostatin-1 along with antioxidants like vitamin and quercetin. Ferroptosis has been considered a potential target for pharmaceutical intervention to alleviate renal IRI-associated cell damage. Thus, this review emphasized the role of ferroptosis and its inhibition in renal IRI. Also, Pharmacological modulation of ferroptosis mechanism in renal I/R injury has been conferred.

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Acknowledgements

The authors extend their appreciation to the Chitkara University Punjab for support.

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Conceptualization: conceived and designed the experiments: Thakur Gurjeet Singh. Analyzed the data: Amarjot Kaur. Wrote the manuscript: Komal Thapa. Visualization: Amarjot Kaur. Editing of the manuscript: Komal Thapa, Amarjot Kaur, and Thakur Gurjeet Singh. Critically reviewed the article: Thakur Gurjeet Singh. Supervision: Thakur Gurjeet Singh. All authors read and approved the final manuscript.

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Correspondence to Thakur Gurjeet Singh.

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Thapa, K., Singh, T.G. & Kaur, A. Targeting ferroptosis in ischemia/reperfusion renal injury. Naunyn-Schmiedeberg's Arch Pharmacol 395, 1331–1341 (2022). https://doi.org/10.1007/s00210-022-02277-5

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  • DOI: https://doi.org/10.1007/s00210-022-02277-5

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