ORIGINAL RESEARCH article
Front. Immunol.
Sec. Alloimmunity and Transplantation
This article is part of the Research TopicCommunity Series in Renal Fibrosis and Renal Transplantation: Vol. IIView all 7 articles
Laptm4a mediates renal ischemia-reperfusion injury by regulating the UNC5B-AKT/mTOR signaling pathway
Provisionally accepted
- Wuhan University Renmin Hospital, Wuhan, China
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Renal ischemia-reperfusion injury (IRI) is a major cause of acute kidney injury (AKI), but specific therapeutic targets are lacking.Lysosomal Protein Transmembrane 4A (LAPTM4A), a four transmembrane-spanning protein mainly localized in endosomes and lysosomes,however, its pathological role in AKI remains unexplored.Here, LAPTM4A is identified as a novel positive mediator of renal IRI. Specifically, the expression of Laptm4a was upregulated in kidney of renal IRI mice and HK2 cells induced by hypoxia-reoxygenation(H/R). Knockout of Laptm4a improved renal function , attenuated tubular injury and reduced inflammatory cell infiltration and apoptosis, whereas overexpression exacerbated the injury.Mechanistically Laptm4a exacerbated renal IRI through suppression of the UNC5B-AKT-mTOR protective signaling pathway.The present study innovatively elucidated the role of Laptm4a as a key positively regulator of IRI, providing a new target for AKI treatment. The clinical significance and targeted intervention strategies of Laptm4a in human AKI need to be further explored in the future.
Keywords: laptm4a, ischemia-reperfusion injury, AKT-mTOR, Inflammation, Apoptosis
Received: 11 Aug 2025; Accepted: 12 Dec 2025.
Copyright: © 2025 MA, Chen, Wang, Chen, Qiu and Zhou. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence:
Tao Qiu
Jiangqiao Zhou
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