Authors
Hongbo Zhang, Ruoxin Tu, Dawei Zhang, Xiangyue Meng, Mengdi Yu, Shuo Ding, Chenhui Ma, Xinyue Qiu, Xiaoqi Yu, Hongna Yin
Published in
Frontiers in neuroscience. Volume 20. Pages 1890903. Epub Jun 30, 2026.
Abstract
PANoptosis is now regarded as an inflammatory form of programmed cell death (PCD). It reflects the coordinated involvement of apoptosis, pyroptosis, and necroptosis, usually through the PANoptosome in a shared pathological environment. This concept may be especially useful in neurological diseases. It helps explain why neuronal death, sustained inflammatory activation, and tissue injury often develop together and reinforce one another. Neural tissue is particularly sensitive to oxidative stress, mitochondrial dysfunction, immune-mediated inflammation, and blood-brain barrier disruption. These pathological changes are common in many forms of neural injury. Therefore, abnormal PANoptosis activation may provide a common mechanism linking different types of nervous system damage. This review summarizes the historical evolution, molecular mechanisms, disease-related roles, and intervention strategies of PANoptosis in neurological disorders. It focuses on PANoptosome assembly and key mechanistic nodes, including NOD-like receptor family pyrin domain-containing 3 (NLRP3), caspase-8, the receptor-interacting serine/threonine protein kinase 1 (RIPK1)/receptor-interacting serine/threonine protein kinase 3 (RIPK3)/mixed lineage kinase domain-like protein (MLKL) axis, gasdermin D (GSDMD), and Ninjurin 1 (NINJ1). It also highlights current translational limitations, such as disease heterogeneity, incomplete cell-specific validation, and insufficient clinical evidence.
PMID:
42453609
Bibliographic data and abstract were imported from PubMed on 17 Sep 2026.
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