Evidence map›Paper›PMID 39215150›Full record

ArticleNature medicine2024

Unidirectional association of clonal hematopoiesis with atherosclerosis development.

Miriam Díez-Díez, Beatriz L Ramos-Neble, Jorge de la Barrera, J C Silla-Castro, Ana Quintas, Enrique Vázquez, M Ascensión Rey-Martín, Benedetta Izzi, Lucía Sánchez-García, Inés García-Lunar and 15 more

Abstract read
In one paragraph

Article in Nature medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

56 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Trial
  3. Article
  4. Cytotoxic CD4Nature aging · 2026
    Article
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Review
  11. Review
  12. Vascular Aging.Circulation · 2026
    Review
  13. Genetic factors contributing to atherosclerosis.Current opinion in cardiology · 2026
    Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

25 authors.

Miriam Díez-Díez *Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0003-1945-825X
Beatriz L Ramos-Neble *Centro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0003-1479-8490
Jorge de la BarreraCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
J C Silla-CastroCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Ana QuintasCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0003-3721-7580
Enrique VázquezCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
M Ascensión Rey-MartínCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Benedetta IzziCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Lucía Sánchez-GarcíaCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Inés García-LunarCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Guiomar MendietaCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Virginia MassCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Nuria Gómez-LópezCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Cristina EspadasCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Gema GonzálezCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Antonio J QuesadaCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0002-3280-8819
Ana García-ÁlvarezCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Antonio Fernández-OrtizCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Enrique Lara-PezziCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.
Ana DopazoCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0002-4910-1684
Fátima Sánchez-CaboCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0003-1881-1664
Borja IbáñezCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0002-5036-254X
Vicente AndrésCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain.ORCID http://orcid.org/0000-0002-0125-7209
Valentín FusterCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain. vfuster@cnic.es.ORCID http://orcid.org/0009-0005-7344-8425
José J FusterCentro Nacional de Investigaciones Cardiovasculares, Madrid, Spain. jjfuster@cnic.es.ORCID http://orcid.org/0000-0002-5970-629X

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Clonal hematopoiesis, a condition in which acquired somatic mutations in hematopoietic stem cells lead to the outgrowth of a mutant hematopoietic clone, is associated with a higher risk of hematological cancer and a growing list of nonhematological disorders, most notably atherosclerosis and associated cardiovascular disease. However, whether accelerated atherosclerosis is a cause or a consequence of clonal hematopoiesis remains a matter of debate. Some studies support a direct contribution of certain clonal hematopoiesis-related mutations to atherosclerosis via exacerbation of inflammatory responses, whereas others suggest that clonal hematopoiesis is a symptom rather than a cause of atherosclerosis, as atherosclerosis or related traits may accelerate the expansion of mutant hematopoietic clones. Here we combine high-sensitivity DNA sequencing in blood and noninvasive vascular imaging to investigate the interplay between clonal hematopoiesis and atherosclerosis in a longitudinal cohort of healthy middle-aged individuals. We found that the presence of a clonal hematopoiesis-related mutation confers an increased risk of developing de novo femoral atherosclerosis over a 6-year period, whereas neither the presence nor the extent of atherosclerosis affects mutant cell expansion during this timeframe. These findings indicate that clonal hematopoiesis unidirectionally promotes atherosclerosis, which should help translate the growing understanding of this condition into strategies for the prevention of atherosclerotic cardiovascular disease in individuals exhibiting clonal hematopoiesis.

Indexed as

AtherosclerosisClonal HematopoiesisMutationAdultFemaleHematopoietic Stem CellsHumansLongitudinal StudiesMaleMiddle Aged

Identifiers

PMID39215150
PMCPMC11485253

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.