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TP53-mediated clonal hematopoiesis confers increased risk for incident atherosclerotic disease

Zekavat, Seyedeh M. (author)
Yale University,Massachusetts Eye and Ear Infirmary,Broad Institute
Viana-Huete, Vanesa (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Matesanz, Nuria (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
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Jorshery, Saman Doroodgar (author)
Massachusetts Institute of Technology
Zuriaga, María A. (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Uddin, Md Mesbah (author)
Broad Institute,Massachusetts General Hospital
Trinder, Mark (author)
Broad Institute,Massachusetts General Hospital,University of British Columbia
Paruchuri, Kaavya (author)
Harvard Medical School,Massachusetts General Hospital,Broad Institute
Zorita, Virginia (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Ferrer-Pérez, Alba (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Amorós-Pérez, Marta (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Kunderfranco, Paolo (author)
Humanitas Research Hospital
Carriero, Roberta (author)
Humanitas Research Hospital
Greco, Carolina M. (author)
Humanitas Research Hospital,Humanitas University
Aroca-Crevillen, Alejandra (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Hidalgo, Andrés (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III,Yale University
Damrauer, Scott M. (author)
University of Pennsylvania,Veterans Health Administration
Ballantyne, Christie M. (author)
Baylor College of Medicine
Niroula, Abhishek (author)
Lund University,Lunds universitet,Hematogenomics,Forskargrupper vid Lunds universitet,Lund University Research Groups,Dana-Farber Cancer Institute,Broad Institute
Gibson, Christopher J. (author)
Dana-Farber Cancer Institute
Pirruccello, James (author)
Broad Institute,Massachusetts General Hospital,University of California, San Francisco
Griffin, Gabriel (author)
Broad Institute,Dana-Farber Cancer Institute,Brigham and Women's Hospital / Harvard Medical School
Ebert, Benjamin L. (author)
Dana-Farber Cancer Institute,Howard Hughes Medical Institute
Libby, Peter (author)
Brigham and Women's Hospital / Harvard Medical School
Fuster, Valentín (author)
Icahn School of Medicine at Mount Sinai,Centro Nacional de Investigaciones Cardiovasculares Carlos III
Zhao, Hongyu (author)
Yale University
Ghassemi, Marzyeh (author)
Massachusetts Institute of Technology
Natarajan, Pradeep (author)
Massachusetts General Hospital,Harvard Medical School,Broad Institute
Bick, Alexander G. (author)
Vanderbilt University
Fuster, José J. (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Klarin, Derek (author)
Stanford University School of Medicine,VA Palo Alto Health Care System
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 (creator_code:org_t)
2023-01-16
2023
English 15 s.
In: Nature Cardiovascular Research. - : Springer Science and Business Media LLC. - 2731-0590. ; 2:2, s. 144-158
Related links:
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  • Journal article (peer-reviewed)
Abstract Subject headings
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  • Somatic mutations in blood indicative of clonal hematopoiesis of indeterminate potential (CHIP) are associated with an increased risk of hematologic malignancy, coronary artery disease and all-cause mortality. Here we analyze the relation between CHIP status and incident peripheral artery disease (PAD) and atherosclerosis, using whole-exome sequencing and clinical data from the UK Biobank and the Mass General Brigham Biobank. CHIP associated with incident PAD and atherosclerotic disease across multiple beds, with increased risk among individuals with CHIP driven by mutation in DNA damage repair (DDR) genes, such as TP53 and PPM1D. To model the effects of DDR-induced CHIP on atherosclerosis, we used a competitive bone marrow transplantation strategy and generated atherosclerosis-prone Ldlr −/− chimeric mice carrying 20% p53-deficient hematopoietic cells. The chimeric mice were analyzed 13 weeks after grafting and showed increased aortic plaque size and accumulation of macrophages within the plaque, driven by increased proliferation of p53-deficient plaque macrophages. In summary, our findings highlight the role of CHIP as a broad driver of atherosclerosis across the entire arterial system beyond the coronary arteries and provide genetic and experimental support for a direct causal contribution of TP53-mutant CHIP to atherosclerosis.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Kardiologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)

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