Evidence map›Paper›PMID 36337911›Full record

ArticleNature cardiovascular research2022

Clonal hematopoiesis in cardiovascular disease and therapeutic implications.

Alan R Tall, Jose J Fuster

Open access · greenAbstract read
In one paragraph

Article in Nature cardiovascular research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
12.9field-weighted citation impact, top 1% of its field
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

57 citing papers in PubMed, 92 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Mathematical modeling ofProceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  6. Article
  7. Article
  8. Observational
  9. Article
  10. Interleukin-18 Inhibition Aggravates Atherosclerosis in Jak2JACC. Basic to translational science · 2026
    Article
  11. Article
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  14. Article
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  17. The DREAM complex links somatic mutation, lifespan, and disease.bioRxiv : the preprint server for biology · 2025
    Article
  18. Article
  19. Review
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 2 institutions in 2 countries.

Alan R TallDivision of Molecular Medicine, Department of Medicine, Columbia University, New York, NY, USA.
Jose J FusterCentro Nacional de Investigaciones Cardiovasculares (CNIC), Madrid, Spain.ORCID 0000-0002-5970-629X
Columbia University · USSpanish National Centre for Cardiovascular Research · ES

Funding

Cholesterol efflux, CHIP and inflammasome activationR01HL107653 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ALAN richard TALL · 2011 to 2026
$7.7M
Clonal hematopoiesis, inflammasomes and atherosclerosisR01HL155431 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI ALAN richard TALL · 2021 to 2026
$3.7M
NHLBI NIH HHS R01 HL107653NHLBI NIH HHS R01 HL155431
6 · The paper itself

Abstract

Clonal hematopoiesis arises from somatic mutations that provide a fitness advantage to hematopoietic stem cells and the outgrowth of clones of blood cells. Clonal hematopoiesis commonly involves mutations in genes that are involved in epigenetic modifications, signaling and DNA damage repair. Clonal hematopoiesis has emerged as a major independent risk factor in atherosclerotic cardiovascular disease, thrombosis and heart failure. Studies in mouse models of clonal hematopoiesis have shown an increase in atherosclerosis, thrombosis and heart failure, involving increased myeloid cell inflammatory responses and inflammasome activation. Although increased inflammatory responses have emerged as a common underlying principle, some recent studies indicate mutation-specific effects. The discovery of the association of clonal hematopoiesis with cardiovascular disease and the recent demonstration of benefit of anti-inflammatory treatments in human cardiovascular disease converge to suggest that anti-inflammatory treatments should be directed to individuals with clonal hematopoiesis. Such treatments could target specific inflammasomes, common downstream mediators such as IL-1β and IL-6, or mutations linked to clonal hematopoiesis.

Identifiers

PMID36337911
PMCPMC9631799
OpenAlexW4210798208

What OpenQuestion holds

Textmetadata
LicenceTDM
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.