Clonal hematopoiesis: the nonhereditary genetics of age-associated cardiovascular disease

Purpose of reviewSomatic mutations, described as noninherited changes in DNA that arise and are passed on to descendant cells, are well known to cause cancers; however, it is increasingly appreciated that the propagation of somatic mutations within a tissue may have a role in causing nonneoplastic disorders and abnormalities in elderly individuals. The nonmalignant clonal expansion of somatic mutations in the hematopoietic system is termed clonal hematopoiesis. This review will briefly discuss how this condition has been linked to various age-related diseases outside the hematopoietic system.Recent findingsClonal hematopoiesis, resulting from leukemic driver gene mutations or mosaic loss of the Y chromosome in leukocytes, is associated with the development of various forms of cardiovascular disease, including atherosclerosis and heart failure, in a mutation-dependent manner.Accumulating evidence shows that clonal hematopoiesis represents a new mechanism for cardiovascular disease and a new risk factor that is as prevalent and consequential as the traditional risk factors that have been studied for decades.

Automated summary

The purpose of this review is to explore the role of somatic mutations in causing nonneoplastic disorders and abnormalities in elderly individuals. Recent findings indicate that clonal hematopoiesis, resulting from leukemic driver gene mutations or mosaic loss of the Y chromosome, is associated with the development of various forms of cardiovascular disease.