细胞焦亡及其在 SARS-CoV-2 感染中的作用。
Pyroptosis and Its Role in SARS-CoV-2 Infection.
机构信息
Department of Immunology, Interfaculty Institute for Cell Biology, University of Tübingen, 72076 Tübingen, Germany.
Department of Radiooncology, Marienhospital Stuttgart, 70199 Stuttgart, Germany.
出版信息
Cells. 2022 May 23;11(10):1717. doi: 10.3390/cells11101717.
The pore-forming inflammatory cell death pathway, pyroptosis, was first described in the early 1990s and its role in health and disease has been intensively studied since. The effector molecule GSDMD is cleaved by activated caspases, mainly Caspase 1 or 11 (Caspase 4/5 in humans), downstream of inflammasome formation. In this review, we describe the molecular events related to GSDMD-mediated pore formation. Furthermore, we summarize the so far elucidated ways of SARS-CoV-2 induced NLRP3 inflammasome formation leading to pyroptosis, which strongly contributes to COVID-19 pathology. We also explore the potential of NLRP3 and GSDMD inhibitors as therapeutics to counter excessive inflammation.
细胞焦亡是一种由炎性小体激活半胱氨酸天冬氨酸蛋白酶（caspase）1/4/5/11 引发的炎症性程序性细胞死亡方式，其特征是细胞迅速肿胀、发生不可逆转的胀亡，并伴随大量促炎症因子的释放。细胞焦亡是机体重要的天然免疫防御机制，在抵抗病原微生物感染中发挥关键作用。2018 年，诺贝尔生理学或医学奖授予了该领域的三位科学家，以表彰他们在细胞焦亡研究领域的杰出贡献。然而，细胞焦亡在缺血再灌注损伤、动脉粥样硬化、神经退行性疾病等多种疾病的发生发展中发挥重要作用。因此，深入研究细胞焦亡的发生机制并探讨靶向细胞焦亡的治疗策略，对于多种疾病的防治具有重要意义。
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