Caspases are a family of conserved cysteine proteases that play key roles in programmed cell death and inflammation. In multicellular organisms, caspases are activated via macromolecular signaling complexes that bring inactive procaspases together and promote their proximity-induced autoactivation and proteolytic processing. Activation of caspases ultimately results in programmed execution of cell death, and the nature of this cell death is determined by the specific caspases involved. Pioneering new research has unraveled distinct roles and cross talk of caspases in the regulation of programmed cell death, inflammation, and innate immune responses. In-depth understanding of these mechanisms is essential to foster the development of precise therapeutic targets to treat autoinflammatory disorders, infectious diseases, and cancer. This review focuses on mechanisms governing caspase activation and programmed cell death with special emphasis on the recent progress in caspase cross talk and caspase-driven gasdermin D-induced pyroptosis.

中文翻译：

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细胞死亡、炎症和细胞焦亡中的半胱天冬酶。

Caspase 是一个保守的半胱氨酸蛋白酶家族，在程序性细胞死亡和炎症中起关键作用。在多细胞生物中，半胱天冬酶通过大分子信号复合物被激活，这些复合物将无活性的半胱天冬酶原聚集在一起并促进它们的邻近诱导的自激活和蛋白水解过程。caspase 的激活最终导致细胞死亡的程序化执行，并且这种细胞死亡的性质由所涉及的特定 caspase 决定。开创性的新研究揭示了半胱天冬酶在调节程序性细胞死亡、炎症和先天免疫反应中的不同作用和相互影响。深入了解这些机制对于开发精确的治疗靶点来治疗自身炎症性疾病、传染病和癌症至关重要。