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REVIEW article
Front. Pharmacol.
Sec. Inflammation Pharmacology
Volume 16 - 2025 | doi: 10.3389/fphar.2025.1559659
This article is part of the Research Topic Targeting Pulmonary Endothelium in Acute Lung Injury and Acute Respiratory Distress Syndrome View all 5 articles
Cell Death In Acute Lung Injury: caspase-regulated apoptosis, pyroptosis, necroptosis, and PANoptosis
Provisionally accepted- Department of Pediatrics, ShengJing Hospital of China Medical University, Shenyang, China
There has been abundant research on the variety of programmed cell death pathways. Apoptosis, pyroptosis, and necroptosis under the action of the caspase family are essential for the innate immune response. Caspases are classified into inflammatory caspase-1/4/5/11, apoptotic caspase-3/6/7, and caspase-2/8/9/10. Although necroptosis is not caspase-dependent to transmit cell death signals, it can cross-link with pyroptosis and apoptosis signals under the regulation of caspase-8. An increasing number of studies have reiterated the involvement of the caspase family in acute lung injuries caused by bacterial and viral infections, blood transfusion, and ventilation, which is influenced by noxious stimuli that activate or inhibit caspase engagement pathways, leading to subsequent lung injury. This article reviews the role of caspases implicated in diverse programmed cell death mechanisms in acute lung injury and the status of research on relevant inhibitors against essential target proteins of the described cell death mechanisms. The findings of this review may help in delineating novel therapeutic targets for acute lung injury.
Keywords: caspase, NLRP3, RIPK, mlkl, Inflammation, Acute Lung Injury
Received: 13 Jan 2025; Accepted: 03 Mar 2025.
Copyright: © 2025 Xiao, Lichuan, Zhang and Hou. 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:
Ana Hou, Department of Pediatrics, ShengJing Hospital of China Medical University, Shenyang, China
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