Journal
THROMBOSIS RESEARCH
Volume 213, Issue -, Pages S107-S112Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.thromres.2021.12.009
Keywords
CHIP; TET2; JAK2; TP53; PPM1D; Inflammation
Categories
Funding
- Ramon y Cajal award - MICIN/AEI [RYC-2016-20026]
- ESF Investing in your future - MICIN/AEI [RTI2018-093554-A-I00]
- ERDF A way of making Europe - Spanish Instituto de Salud Carlos III as part of the European Research Area Network on Cardiovascular Diseases CHEMICAL [AC19/00133]
- Leducq Foundation [TNE-18CVD04]
- MICIN
- Pro-CNIC Foundation
- MICIN/AEI [CEX2020-001041-S]
- Instituto de Salud Carlos III
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Somatic mutations are not only common in cancer, but also present in non-cancerous cells, particularly in the hematopoietic system. Clonal hematopoiesis, driven by certain mutations, is associated with a higher risk of hematological malignancies and may also contribute to the development of cardiovascular disease.
Cancer genomes have long been known to carry a high number of somatic mutations distributed across many genes. However, recent sequencing studies have unveiled that non-cancerous cells also carry a considerable number of somatic mutations, which are acquired continuously through the lifespan. Accordingly, the pathophysiological relevance of somatic mutagenesis beyond cancer has become a topic of intensive research. Human genetic studies and experiments in mice have shown that some somatic mutations in the hematopoietic system provide a competitive advantage to the mutant cell and allow its clonal expansion. This phenomenon, termed clonal hematopoiesis, is typically driven by mutations in known oncogenes and tumor suppressor genes, and it is associated with a higher risk of hematological malignancies. Unexpectedly, accumulating genetic and experimental evidence strongly suggest that clonal hematopoiesis, at least when driven by certain mutations, also contributes causally to the development of cardiovascular disease and, therefore, represents a new cardiovascular risk factor. While clonal hematopoiesis is relatively common in healthy individuals, especially among the elderly, it is particularly frequent in cancer patients and survivors. Hence, it has emerged as a candidate contributor to the increased risk of cardiovascular complications in cancer patients. This review summarizes our current understanding of the connection between clonal hematopoiesis and cardiovascular disease, with a special focus on the available evidence linking clonal hematopoiesis to cardiovascular disorders that are frequent in cancer patients and survivors.
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