细胞经历一种称为“火性凋亡”（注：pyroptosis，带有希腊语词根“火”）的炎症编程性溶解性细胞死亡，常常表现出大型膨胀突起和随后爆裂等形态学特征。最初被描述为对细菌感染产生依赖caspase-1的细胞死亡，2018年重新定义为依赖于细胞质膜孔的一种细胞死亡，该膜孔由气体死亡素（GSDM）家族成员产生[1,2]。GSDMs在质膜和细胞器膜中形成孔结构，从而引发膜破坏和细胞的迅速溶解性死亡。在感染、炎症、肿瘤发病机制和抗肿瘤疗法的背景下，气体死亡素家族在火性凋亡的执行中起着重要作用。最近，一些GSDMs被提出具有细胞死亡无关的功能。因此，全面了解GSDM基因调控，包括在稳态条件和炎症期间的机制，是必要的。在本综述中，我们将总结GSDMs在火性凋亡中的作用，并重点讨论调控GSDMs表达的转录和表观遗传机制。Copyright © 2023 Elsevier Ltd. All rights reserved.

Cells undergo an inflammatory programmed lytic cell death called 'pyroptosis' (with the Greek roots 'fiery'), often featuring morphological hallmarks such as large ballooning protrusions and subsequent bursting. Originally described as a caspase-1-dependent cell death in response to bacterial infection, pyroptosis has since been re-defined in 2018 as a cell death dependent on plasma membrane pores by a gasdermin (GSDM) family member [1,2]. GSDMs form pores in the plasma membrane as well as organelle membranes, thereby initiating membrane destruction and the rapid and lytic demise of a cell. The gasdermin family plays a profound role in the execution of pyroptosis in the context of infection, inflammation, tumor pathogenesis, and anti-tumor therapy. More recently, cell-death-independent functions for some of the GSDMs have been proposed. Therefore, a comprehensive understanding of gasdermin gene regulation, including mechanisms in both homeostatic conditions and during inflammation, is essential. In this review, we will summarize the role of gasdermins in pyroptosis and focus our discussion on the transcriptional and epigenetic mechanisms controlling the expression of GSDMs.Copyright © 2023 Elsevier Ltd. All rights reserved.