Platelet intrinsic apoptosis

Emma C Josefsson

doi:10.1016/j.thromres.2022.11.024

Platelet intrinsic apoptosis

Thromb Res. 2023 Nov:231:206-213. doi: 10.1016/j.thromres.2022.11.024. Epub 2022 Dec 12.

Author

Emma C Josefsson¹

Affiliation

¹ 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. Electronic address: emma.josefsson@gu.se.

PMID: 36739256
DOI: 10.1016/j.thromres.2022.11.024

Abstract

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_L 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.

Keywords: Apoptosis; BCL-X(L); Cell death; Lifespan; Mitochondria; Platelet.

Publication types

Review

MeSH terms

Apoptosis*
Blood Platelets* / metabolism
Humans
bcl-2-Associated X Protein / metabolism
bcl-X Protein / metabolism

Substances

bcl-2-Associated X Protein
bcl-X Protein