2026-06-14T03:53:16Zhttps://repisalud.isciii.es/rest/oai/requestoai:repisalud.isciii.es:20.500.12105/168122024-09-27T08:09:08Zcom_20.500.12105_19604com_20.500.12105_2051col_20.500.12105_19605
Repisalud
author
Zuriaga, María A
author
Fuster, Jose J.
2023-12-15T09:40:12Z
2023-12-15T09:40:12Z
2023
Clin Investig Arterioscler. 2023 Jan-Feb;35(1):35-41.
10.1016/j.arteri.2021.09.006
1578-1879
Clinica e investigacion en arteriosclerosis : publicacion oficial de la Sociedad Espanola de Arteriosclerosis
34879980
http://hdl.handle.net/20.500.12105/16812
Despite current standards of care, a considerable risk of atherosclerotic cardiovascular disease remains in both primary and secondary prevention. In this setting, clonal hematopoiesis driven by somatic mutations has recently emerged as a relatively common, potent and independent risk factor for atherosclerotic cardiovascular disease and other cardiovascular conditions. Experimental studies in mice suggest that mutations in TET2 and JAK2, which are among the most common in clonal hematopoiesis, increase inflammation and are causally connected to accelerated atherosclerosis development, which may explain the link between clonal hematopoiesis and increased cardiovascular risk. In this review, we provide an overview of our current understanding of this emerging cardiovascular risk factor.
eng
Clonal hematopoiesis and atherosclerotic cardiovascular disease: A primer.
journal article
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Clonal hematopoiesis_Clin Investig Arterioscler_2023.pdf
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Clonal hematopoiesis_Clin Investig Arterioscler_2023.pdf.txt