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REVIEW article

Front. Immunol.

Sec. Alloimmunity and Transplantation

Volume 16 - 2025 | doi: 10.3389/fimmu.2025.1553298

This article is part of the Research Topic Multi-omics Assessment for the Discovery of Promising Novel Molecules in the Treatment of Transplant Organ Injury View all 3 articles

Protein modifications in hepatic ischemia-reperfusion injury: molecular mechanisms and targeted therapy

Provisionally accepted
XiaoHong Zhao XiaoHong Zhao Qinyi Li Qinyi Li Xiaolong Zhu Xiaolong Zhu Yuanyuan Jiao Yuanyuan Jiao Huan Yang Huan Yang Jiao Feng Jiao Feng *
  • Hangzhou Normal University, Hangzhou, China

The final, formatted version of the article will be published soon.

    Ischemia-reperfusion injury refers to the damage that occurs when blood supply is restored to organs or tissues after a period of ischemia. This phenomenon is commonly observed in clinical contexts such as organ transplantation and cardiac arrest resuscitation. Among these, hepatic ischemiareperfusion injury is a prevalent complication in liver transplantation, significantly impacting the functional recovery of the transplanted liver and potentially leading to primary graft dysfunction.With the growing demand for organ transplants and the limited availability of donor organs, effectively addressing hepatic ischemia-reperfusion injury is essential for enhancing transplantation success rates, minimizing complications, and improving graft survival. The pathogenesis of hepatic ischemia-reperfusion injury is multifaceted, involving factors such as oxidative stress and inflammatory responses. This article focuses on the role of protein post-translational modifications in hepatic ischemia-reperfusion injury, including phosphorylation, ubiquitination, acetylation, ADPribosylation, SUMOylation, crotonylation, palmitoylation, and S-nitrosylation. Initially, we examined the historical discovery of these protein post-translational modifications and subsequently investigated their impact on cellular signal transduction, enzymatic activity, protein stability, and protein-protein interactions. The emphasis of this study is on the pivotal role of protein posttranslational modifications in the progression of hepatic ischemia-reperfusion injury and their potential as therapeutic targets. This study aims to conduct a comprehensive analysis of recent advancements in research on protein modifications in hepatic ischemia-reperfusion injury, investigate the underlying molecular mechanisms, and explore future research trajectories. Additionally, future research directions are proposed, including the exploration of interactions between various protein modifications, the identification of specific modification sites, and the development of drugs targeting these modifications. These efforts aim to deepen our understanding of protein posttranslational modifications in hepatic ischemia-reperfusion injury and pave the way for innovative therapeutic interventions.

    Keywords: Liver Transplantation, Hepatic ischemia-reperfusion injury, post-translational modification, targeted therapy, Inflammatory Response

    Received: 30 Dec 2024; Accepted: 17 Mar 2025.

    Copyright: © 2025 Zhao, Li, Zhu, Jiao, Yang and Feng. 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: Jiao Feng, Hangzhou Normal University, Hangzhou, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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