The Mechanism of G Protein-Coupled Receptor Regulation of Ferroptosis in Hepatic Ischemia–Reperfusion Injury

TL;DR

This paper reviews how G protein-coupled receptors influence ferroptosis in liver injury during surgery and transplantation.

Contribution

It provides a detailed review of molecular mechanisms linking GPCRs to ferroptosis in hepatic ischemia–reperfusion injury.

Findings

GPCRs regulate ferroptosis through lipid peroxidation and iron metabolism pathways.

Targeting GPCRs may offer therapeutic strategies to reduce liver injury.

The review highlights antioxidant defense as a key modulator in this process.

Abstract

Hepatic ischemia–reperfusion injury (HIRI) is a significant clinical challenge in the field of liver surgery and transplantation, and its pathological mechanisms are complex. In recent years, ferroptosis, a novel form of iron-dependent programmed cell death, plays a central role in this injury process. G protein-coupled receptors (GPCRs), as the largest family of membrane receptors in the body, regulate cellular stress and death through extensive signaling networks. This review elucidates the specific molecular mechanisms by which GPCRs regulate ferroptosis in HIRI by affecting key pathways such as lipid peroxidation, iron metabolism homeostasis, and antioxidant defense. It further explores potential therapeutic strategies targeting specific GPCRs to modulate ferroptosis, thereby alleviating liver injury and improving postoperative outcomes, to provide new insights and a theoretical basis for clinical translation.

Figures