Open AccessClonal hematopoiesis driven by DNMT3A and TET2 mutations: role in monocyte and macrophage biology and atherosclerotic cardiovascular disease
Author(s) -
Isidoro Cobo,
Tiffany Tanaka,
Christopher K. Glass,
Calvin Yeang
Publication year - 2021
Publication title -
current opinion in hematology/current opinion in hematology, with evaluated medline
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.295
H-Index - 97
eISSN - 1080-8213
pISSN - 1065-6251
DOI - 10.1097/moh.0000000000000688
Subject(s) - epigenetics , dna methylation , biology , haematopoiesis , myeloid , immune system , immunology , somatic cell , disease , context (archaeology) , monocyte , cancer research , genetics , gene , medicine , gene expression , stem cell , paleontology
Clonal hematopoiesis of indeterminate potential (CHIP), defined by the presence of somatic mutations in hematopoietic cells, is associated with advanced age and increased mortality due to cardiovascular disease. Gene mutations in DNMT3A and TET2 are the most frequently identified variants among patients with CHIP and provide selective advantage that spurs clonal expansion and myeloid skewing. Although DNMT3A and TET2 appear to have opposing enzymatic influence on DNA methylation, mounting data has characterized convergent inflammatory pathways, providing insights to how CHIP may mediate atherosclerotic cardiovascular disease (ASCVD).