脓毒症中的半胱氨酸天冬氨酸蛋白酶和程序性细胞死亡：机制、病理生理学和治疗靶点
Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.
摘要(中文译文)
脓毒症是一种危重的医学状态，其特征是机体对病原体感染产生失控的全身性反应而导致器官功能障碍，给重症监护管理带来巨大困难。作为关键病理机制，程序性细胞死亡（PCD）对脓毒症的发生发展起重要促进作用，而半胱天冬酶（caspases）是调控多种PCD形式的核心分子枢纽，包括凋亡、坏死性凋亡、焦亡和PANoptosis。本文综述了半胱天冬酶的分类与结构特征，阐述了其在调控四条PCD通路中的分子机制，并阐明了这些PCD形式在脓毒症所致免疫失调和器官损伤中的双重病理作用。我们还总结了靶向半胱天冬酶的治疗策略，为开发脓毒症新型靶向治疗提供理论依据。
Abstract
Sepsis represents a critical medical condition characterized by organ impairment resulting from an uncontrolled systemic reaction to pathogenic infection, posing substantial difficulties in intensive care management. As a key pathological mechanism, programmed cell death (PCD) critically contributes to sepsis development, and caspases act as the central molecular hub governing multiple PCD modalities, including apoptosis, necroptosis, pyroptosis, and PANoptosis. In this manuscript, we review the classification and structural features of caspases, illustrate their molecular mechanisms in regulating the four PCD pathways, and clarify the dual pathological roles of these PCD forms in sepsis-induced immune dysregulation and organ damage. We also summarize therapeutic strategies targeting caspases and provide a theoretical basis for developing novel targeted treatments for sepsis.
如何引用
AMA
Haibei He, Xiuli Xie, Lisui Zhou, Yumeng Lin, Aijun Liu, Peng Guo, et al. Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.. Frontiers in immunology. 2026; doi:10.3389/fimmu.2026.1879033.
APA
Haibei He, Xiuli Xie, Lisui Zhou, Yumeng Lin, Aijun Liu, Peng Guo, et al (2026). Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.. Frontiers in immunology. https://doi.org/10.3389/fimmu.2026.1879033
GB/T 7714
Haibei He, Xiuli Xie, Lisui Zhou, Yumeng Lin, Aijun Liu, Peng Guo, et al. Caspases and programmed cell death in sepsis: mechanisms, pathophysiology, and therapeutic targets.[J]. Frontiers in immunology, 2026 doi:10.3389/fimmu.2026.1879033.
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