焦亡、气体酶及过敏性疾病
Pyroptosis, gasdermins and allergic diseases
DOI 原文链接
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影响因子:12
分区:医学1区 Top / 过敏1区 免疫学1区
发表日期:2024 Sep
作者:
Ronald Allan Panganiban, Kari C Nadeau, Quan Lu
DOI:
10.1111/all.16236
摘要
焦亡是一种炎症性程序性细胞死亡形式，区别于坏死和凋亡。焦亡主要由气体酶家族（GSDMA-E及PVJK）介导，当被蛋白酶裂解激活后，形成细胞膜孔，导致细胞死亡。尽管过去关于焦亡的研究多集中在其在癌症、代谢紊乱和感染性疾病中的作用，近期的实验和观察性研究开始将焦亡与过敏性疾病联系起来。这些研究表明，气体酶介导的焦亡促成了过敏症的发生，并可能提供新的治疗靶点。本文综述了我们对焦亡的现有理解，重点强调气体酶作为焦亡执行者及潜在的过敏性疾病介质的作用。我们突出报道了气体酶生化作用与过敏疾病发生之间的机制联系的新发现。此外，讨论焦亡及气体酶如何可能影响上皮屏障功能障碍——这是被认为引发多种过敏疾病进展的关键因素。
Abstract
Pyroptosis is an inflammatory form of programmed cell death that is distinct from necrosis and apoptosis. Pyroptosis is primarily mediated by the gasdermin family of proteins (GSDMA-E and PVJK), which, when activated by proteolytic cleavage, form pores in the plasma membrane, leading to cell death. While much of the past research on pyroptosis has focused on its role in cancer, metabolic disorders, and infectious diseases, recent experimental and observational studies have begun to implicate pyroptosis in allergic diseases. These studies suggest that gasdermin-mediated pyroptosis contributes to the development of allergic conditions and could offer novel targets for therapy. Here, we review our current understanding of pyroptosis with an emphasis on the role of gasdermins as executioners of pyroptosis and potential mediators to allergic disease. We highlight new discoveries that establish a mechanistic link between the biochemical actions of gasdermins and the onset of allergic diseases. Additionally, we discuss how pyroptosis and gasdermins might contribute to the dysfunction of epithelial barrier, a key factor believed to initiate the progression of various allergic diseases.