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

Zekavat, Seyedeh M. (author)
Broad Institute,Yale University,Massachusetts Eye and Ear Infirmary
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)
Massachusetts General Hospital,Broad Institute
Trinder, Mark (author)
University of British Columbia,Massachusetts General Hospital,Broad Institute
Paruchuri, Kaavya (author)
Massachusetts General Hospital,Harvard Medical School,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 University,Humanitas Research Hospital
Aroca-Crevillen, Alejandra (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Hidalgo, Andrés (author)
Yale University,Centro Nacional de Investigaciones Cardiovasculares Carlos III
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,Broad Institute,Dana-Farber Cancer Institute
Gibson, Christopher J. (author)
Dana-Farber Cancer Institute
Pirruccello, James (author)
Broad Institute,University of California, San Francisco,Massachusetts General Hospital
Griffin, Gabriel (author)
Broad Institute,Brigham and Women's Hospital / Harvard Medical School,Dana-Farber Cancer Institute
Ebert, Benjamin L. (author)
Howard Hughes Medical Institute,Dana-Farber Cancer Institute
Libby, Peter (author)
Brigham and Women's Hospital / Harvard Medical School
Fuster, Valentín (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III,Icahn School of Medicine at Mount Sinai
Zhao, Hongyu (author)
Yale University
Ghassemi, Marzyeh (author)
Massachusetts Institute of Technology
Natarajan, Pradeep (author)
Harvard Medical School,Broad Institute,Massachusetts General Hospital
Bick, Alexander G. (author)
Vanderbilt University
Fuster, José J. (author)
Centro Nacional de Investigaciones Cardiovasculares Carlos III
Klarin, Derek (author)
VA Palo Alto Health Care System,Stanford University School of Medicine
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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:
http://dx.doi.org/10...
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https://lup.lub.lu.s...
https://doi.org/10.1...
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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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