The clonal hematopoiesis mutation Jak2^V617F aggravates endothelial injury and thrombosis in arteries with erosion-like intimas.

ABSTRACT:

Background

Superficial plaque erosion causes many acute coronary syndromes. However, mechanisms of plaque erosion remain poorly understood, and we lack directed therapeutics for thrombotic complication. Human eroded plaques can harbor neutrophil extracellular traps (NETs) that propagate endothelial damage at experimental arterial lesions that recapitulate superficial erosion. Clonal Hematopoiesis of Indeterminate Potential (CHIP) denotes age-related clonal expansion of bone marrow-derived cells harboring somatic mutations in the absence of overt hematological disease. CHIP heightens the risk of cardiovascular disease, with the greatest increase seen in individuals with JAK2^V617F. Neutrophils from mice and humans with JAK2^V617F undergo NETosis more readily than

SUBMITTER: Molinaro R 

PROVIDER: S-EPMC11753411 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature