Abstract
Background and Aims : Acquired mutations in hematopoietic cells that lead to clonal hematopoiesis (CH) are emerging as new drivers of atherosclerotic cardiovascular disease. The TP53 gene, which encodes the tumor suppressor protein p53, is one of the most frequently mutated genes in individuals exhibiting CH. Here, we investigated the effects of CH driven by inactivating mutations in p53 on experimental atherosclerosis development.
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