A cell death ballet in two acts

IF 47.3 1区综合性期刊 Q1 MULTIDISCIPLINARY SCIENCES

Science Pub Date : 2026-10-22 DOI:10.1126/science.aem1247

Cristina Muñoz-Pinedo, Seamus J. Martin

引用次数: 0

Abstract

Complex multicellular organisms require ongoing replacement of cells for many reasons, including aging, infection, and injury. In many situations, cell death occurs in response to stress through a regulated process called apoptosis (1). A key pathway to apoptosis involves two related proteins, Bcl-2–associated X protein (BAX) and Bcl-2–homologous antagonist killer (BAK), that form pores in mitochondria (2, 3). This releases cytochrome c into the cytosol to trigger activation of caspase proteases that coordinate apoptosis (4). BAX-BAK pores can also lead to delayed release of mitochondrial DNA (mtDNA) into the cytosol and the production of type I interferons (IFNs), which is a classical antiviral immune response (5, 6). On page 401 of this issue, Yang et al. (7) report two distinct BAX-BAK complexes—one for cytochrome c release that promotes immunologically silent caspase-dependent apoptosis and another that promotes mtDNA release, caspase-independent cell death, and IFN production to stimulate inflammation.

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两幕细胞死亡芭蕾

复杂的多细胞生物需要不断更换细胞的原因有很多，包括老化、感染和损伤。在许多情况下，细胞死亡是对应激的反应，通过一个被称为细胞凋亡的调节过程发生(1)。凋亡的关键途径涉及两个相关蛋白，bcl -2相关X蛋白（BAX）和bcl -2同源拮抗剂杀手（BAK），它们在线粒体中形成孔隙（2,3）。这将细胞色素c释放到细胞质中，触发协调细胞凋亡的半胱天冬酶蛋白酶的激活(4)。BAX-BAK孔也可以导致线粒体DNA （mtDNA）延迟释放到细胞质中，并产生I型干扰素（ifn），这是一种经典的抗病毒免疫反应（5,6）。在本期的401页上，Yang等人(7)报道了两种不同的BAX-BAK复合物——一种促进细胞色素c释放，促进免疫沉默的caspase依赖性细胞凋亡，另一种促进mtDNA释放，caspase非依赖性细胞死亡和IFN产生，以刺激炎症。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Science 综合性期刊-综合性期刊

CiteScore

61.10

自引率

0.90%

发文量

审稿时长

2.1 months

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