Nature Communications (Sep 2022)

Clonal hematopoiesis of indeterminate potential, DNA methylation, and risk for coronary artery disease

  • M d Mesbah Uddin,
  • Ngoc Quynh H. Nguyen,
  • Bing Yu,
  • Jennifer A. Brody,
  • Akhil Pampana,
  • Tetsushi Nakao,
  • Myriam Fornage,
  • Jan Bressler,
  • Nona Sotoodehnia,
  • Joshua S. Weinstock,
  • Michael C. Honigberg,
  • Daniel Nachun,
  • Romit Bhattacharya,
  • Gabriel K. Griffin,
  • Varuna Chander,
  • Richard A. Gibbs,
  • Jerome I. Rotter,
  • Chunyu Liu,
  • Andrea A. Baccarelli,
  • Daniel I. Chasman,
  • Eric A. Whitsel,
  • Douglas P. Kiel,
  • Joanne M. Murabito,
  • Eric Boerwinkle,
  • Benjamin L. Ebert,
  • Siddhartha Jaiswal,
  • James S. Floyd,
  • Alexander G. Bick,
  • Christie M. Ballantyne,
  • Bruce M. Psaty,
  • Pradeep Natarajan,
  • Karen N. Conneely

DOI
https://doi.org/10.1038/s41467-022-33093-3
Journal volume & issue
Vol. 13, no. 1
pp. 1 – 16

Abstract

Read online

Clonal hematopoiesis, often caused by mutations in DNMT3A and TET2, is associated with blood cancer and coronary artery disease. Here, the authors conduct an epigenome-wide association study, finding that clonal hematopoiesis caused by DNMT3A vs. TET2 mutations has directionally opposing changes in DNA methylation profiles, with both promoting stem cell self-renewal.