Josefsson Emma C
Sahlgrenska University Hospital, Department of Clinical Chemistry, Gothenburg, Sweden; The University of Gothenburg, Department of Laboratory Medicine, Institute of Biomedicine, Gothenburg, Sweden; The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, VIC 3052, Australia; The University of Melbourne, Department of Medical Biology, 1G Royal Parade, VIC 3052, Australia.
Thromb Res. 2023 Nov;231:206-213. doi: 10.1016/j.thromres.2022.11.024. Epub 2022 Dec 12.
In a healthy individual, the lifespan of most platelets is tightly regulated by intrinsic, or mitochondrial, apoptosis. This is a special form of programmed cell death governed by the BCL-2 family of proteins, where the prosurvival protein BCL-X maintains platelet viability by restraining the prodeath proteins BAK and BAX. Restriction of platelet lifespan by activation of BAK and BAX mediated intrinsic apoptosis is essential to maintain a functional, haemostatically reactive platelet population. This review focuses on the molecular regulation of intrinsic apoptosis in platelets, reviews conditions linked to enhanced platelet death, discusses ex vivo storage of platelets and describes caveats associated with the assessment of platelet apoptosis.
在健康个体中，大多数血小板的寿命由内在凋亡（即线粒体凋亡）严格调控。这是一种由BCL-2蛋白家族控制的程序性细胞死亡的特殊形式，其中促生存蛋白BCL-X通过抑制促死亡蛋白BAK和BAX来维持血小板的存活。通过激活BAK和BAX介导的内在凋亡来限制血小板寿命对于维持功能性、具有止血反应性的血小板群体至关重要。本文综述聚焦于血小板内在凋亡的分子调控，回顾与血小板死亡增强相关的情况，讨论血小板的体外储存，并描述与血小板凋亡评估相关的注意事项。
