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Review | Open Access

PANoptosis: a new insight into the mechanism of ischaemia–reperfusion injury

Huapei Song‡ , Guangping Liang‡, Fengjun Wang( )
Institute of Burn Research, The First Affiliated Hospital of Army Medical University (The Third Military Medical University), State Key Laboratory of Trauma and Chemical Poisoning, Gaotanyan Street, Shapingba Disdrict, Chongqing 400038, China

‡These authors contributed equally to this work.

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Highlights

• This is the first to review the role of PANoptosis in ischaemia–reperfusion injury (IRI), which might be helpful to clarify the function and mechanism of PANoptosis in tissue IRI after severe burns.

• This review systematically described the emergence, clinical evidence, molecular mechanisms of PANoptosis, and its role in IRI.

Abstract

Programmed cell death, which occurs via modes such as apoptosis, necroptosis, and pyroptosis, is an important mechanism for host defence against pathogens and inflammation-mediated immune responses. Recently, interactions between various types of cell death have gradually been discovered. PANoptosis is a newly discovered mode of programmed cell death that involves apoptosis, necroptosis, and pyroptosis and is closely related to many diseases. Ischaemia–reperfusion injury (IRI) is common in patients with blood circulation disorders such as those related to burns, traumatic shock, surgery, organ transplantation, and thrombus. However, the literature on the role of PANoptosis in IRI is limited. Herein, we systematically described the emergence of PANoptosis as a cell death mode, clinical evidence of its occurrence, the molecular mechanisms of PANoptosis, and its role in IRI. This study is expected to provide novel approaches for the prevention and treatment of tissue and organ IRI after severe burns.

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Burns & Trauma
Article number: tkaf026

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Cite this article:
Song H, Liang G, Wang F. PANoptosis: a new insight into the mechanism of ischaemia–reperfusion injury. Burns & Trauma, 2025, 13(7): tkaf026. https://doi.org/10.1093/burnst/tkaf026

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Received: 16 February 2025
Revised: 06 April 2025
Accepted: 07 April 2025
Published: 10 October 2026
© The Author(s) 2025. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.