Ontology highlight
ABSTRACT: Background
Aging is an independent risk factor for the development of cardiovascular, thrombotic, and other chronic diseases. However, mechanisms of platelet hyperactivation in aging remain poorly understood.Objectives
Here, we examine whether and how aging alters intracellular signaling in platelets to support platelet hyperactivity and thrombosis.Methods
Quantitative mass spectrometry with tandem mass tag labeling systematically measured protein phosphorylation in platelets from healthy aged (>65 years) and young human (<45 years) subjects. The role of platelet mechanistic target of rapamycin (mTOR) in aging-induced platelet hyperreactivity was assessed using pharmacologic mTOR inhibition and a platelet-specific mTOR-deficient mouse model (mTORplt-/-).<
SUBMITTER: Portier I
PROVIDER: S-EPMC11656450 | biostudies-literature | 2024 Sep
REPOSITORIES: biostudies-literature