Evidence map›Paper›PMID 41492475›Full record

ArticleGenes & diseases2026

Selenoprotein GPX3 regulates NADPH oxidase expression by inhibiting the MAPK signaling pathway and thereby attenuating the inflammatory response in renal ischemia-reperfusion injury.

Jun Pei, Jie Zhang, Chengjun Yu, Jin Luo, Sheng Wen, Yi Hua, Guanghui Wei

Abstract read
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Article in Genes & diseases, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

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1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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3 · Its place in the literature

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1 citing paper in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

7 authors.

Jun PeiDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Jie ZhangDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Chengjun YuDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Jin LuoDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Sheng WenDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Yi HuaDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.
Guanghui WeiDepartment of Urology, Children's Hospital of Chongqing Medical University, Chongqing 400014, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Renal ischemia-reperfusion injury (IRI) is one of the major causes of acute kidney injury, and the inflammatory response is considered a key factor. The selenoprotein GPX3, a member of the glutathione peroxidase family, has gradually attracted attention for its anti-inflammatory properties. However, the relationship between GPX3 and the inflammatory response during renal IRI remains unclear. The present study aims to investigate the role of GPX3 on the inflammatory response during renal IRI and related mechanisms. We utilized classic rat models of kidney IRI and cellular hypoxia reoxygenation model. After overexpressing GPX3 via lentiviruses and adeno-associated viruses, we observed a significant reduction in the expression levels of inflammatory factors in renal tissues, along with an increase in the expression of anti-inflammatory factor IL-10, resulting in noticeable alleviation of renal IRI. Meanwhile, we found that GPX3 alleviated the inflammatory response, probably by inhibiting the MAPK signaling pathway and reducing the expression of NAPDH oxidase. To further validate the mechanism by which GPX3 alleviated the inflammatory response, we used the MAPK signaling pathway agonist anisomycin for intervention. The results showed that anisomycin intervention significantly reversed the inhibitory effect of GPX3 on the MAPK signaling pathway, in which the expression level of NADPH oxidase was significantly increased, the secretion of inflammatory factors was increased, and the degree of renal tissue damage was significantly increased. These findings suggest that selenoprotein GPX3 alleviates inflammation during renal IRI by inhibiting the MAPK signaling pathway and reducing NADPH oxidase expression.

Indexed as

GPX3InflammationIschemia-reperfusion injuryKidneySelenoprotein

Identifiers

PMID41492475
PMCPMC12765255

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.