The mitochondrial caspase cascade was originally thought to be required for apoptotic death driven by Bak/Bax-mediated intrinsic apoptosis. It has also been ascribed several ‘non-apoptotic’ functions, including differentiation, proliferation, and cellular reprogramming. Recent work has demonstrated that, during apoptosis, the caspase cascade suppresses damage-associated molecular pattern (DAMP)-initiated production of cytokines such as type I interferon by the dying cell. The caspase cascade is not required for death to occur; instead, it shapes the immunogenic properties of the apoptotic cell. This raises questions about the role of apoptotic caspases in regulating DAMP signaling more generally, puts a new perspective on their non-apoptotic functions, and suggests that pharmacological caspase inhibitors might find new applications as antiviral or anticancer agents.

最初认为线粒体半胱天冬酶级联是由Bak / Bax介导的内在凋亡导致的凋亡死亡所必需的。它还被归类为几种“非凋亡”功能，包括分化，增殖和细胞重编程。最近的研究表明，在凋亡过程中，半胱天冬酶级联抑制了死亡细胞对损伤相关分子模式（DAMP）的细胞因子（例如I型干扰素）的产生。发生死亡不需要caspase级联；相反，它改变了凋亡细胞的免疫原性。这引发了有关凋亡半胱天冬酶在更广泛的调节DAMP信号传导中作用的疑问，为它们的非凋亡功能提供了新的视角，