焦亡是一种新的炎症性程序性细胞死亡 (PCD) 类型，通常由多种炎症小体触发，这些炎症小体可以识别不同的危险或损伤相关分子模式 (DAMP)，从而导致 caspase-1 的激活和gasdermin D 的裂解（GSDMD）。 Gasdermin 家族成孔蛋白是细胞焦亡的执行者，通常通过自身抑制维持在非活性状态。在半胱天冬酶介导的 Gasdermin 裂解后，促焦亡的 N 端片段从 C 端片段的自动抑制中释放出来并寡聚化，在质膜中形成孔。这导致白细胞介素 (IL)-1β、IL-18 和高迁移率族蛋白 1 (HMGB1) 的分泌，产生渗透性膨胀和裂解。目前肺癌的治疗方法包括化疗、放疗、分子靶向治疗和免疫治疗，有效迫使癌细胞发生焦亡，从而产生局部和全身的抗肿瘤免疫。因此，焦亡被认为是治疗肺癌的新治疗方案。在这篇综述中，我们简要描述了焦亡所涉及的信号通路，并努力讨论焦亡的抗肿瘤作用及其在肺癌治疗中的潜在应用，重点关注焦亡对微环境重编程和唤起抗肿瘤免疫反应的贡献。© 2024威利期刊有限责任公司。

Pyroptosis, a newly characterized type of inflammatory programmed cell death (PCD), is usually triggered by multiple inflammasomes which can recognize different danger or damage-associated molecular patterns (DAMPs), leading to the activation of caspase-1 and the cleavage of gasdermin D (GSDMD). Gasdermin family pore-forming proteins are the executers of pyroptosis and are normally maintained in an inactive state through auto-inhibition. Upon caspases mediated cleavage of gasdermins, the pro-pyroptotic N-terminal fragment is released from the auto-inhibition of C-terminal fragment and oligomerizes, forming pores in the plasma membrane. This results in the secretion of interleukin (IL)-1β, IL-18, and high-mobility group box 1 (HMGB1), generating osmotic swelling and lysis. Current therapeutic approaches including chemotherapy, radiotherapy, molecularly targeted therapy and immunotherapy for lung cancer treatment efficiently force the cancer cells to undergo pyroptosis, which then generates local and systemic antitumor immunity. Thus, pyroptosis is recognized as a new therapeutic regimen for the treatment of lung cancer. In this review, we briefly describe the signaling pathways involved in pyroptosis, and endeavor to discuss the antitumor effects of pyroptosis and its potential application in lung cancer therapy, focusing on the contribution of pyroptosis to microenvironmental reprogramming and evocation of antitumor immune response.© 2024 Wiley Periodicals LLC.