Evidence map›Paper›PMID 33861346›Full record

ReviewClinical science (London, England : 1979)2021

Clonal haematopoiesis of indeterminate potential: intersections between inflammation, vascular disease and heart failure.

Leanne Mooney, Carl S Goodyear, Tamir Chandra, Kristina Kirschner, Mhairi Copland, Mark C Petrie, Ninian N Lang

Open access · hybridAbstract readReview
In one paragraph

Review in Clinical science (London, England : 1979), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
  2. The immunology behind inflammaging-causes, sources, and mechanisms.The Journal of allergy and clinical immunology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Observational
  8. Article
  9. Review
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Review
  16. Modern Concepts in Cardiovascular Disease: Inflamm-Aging.Frontiers in cell and developmental biology · 2022
    Review
  17. Review
  18. Review
  19. Article
  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

7 authors at 4 institutions in 2 countries.

Leanne MooneyBHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, U.K.
Carl S GoodyearInstitute of Immunity, Infection and Inflammation, University of Glasgow, Glasgow, U.K.
Tamir ChandraThe Institute of Genetics and Molecular Medicine, University of Edinburgh, Western General Hospital, Crewe Road, Edinburgh, U.K.
Kristina KirschnerPaul O'Gorman Leukaemia Research Centre, Institute for Cancer Science, University of Glasgow, Glasgow, U.K.
Mhairi CoplandPaul O'Gorman Leukaemia Research Centre, Institute for Cancer Science, University of Glasgow, Glasgow, U.K.
Mark C PetrieBHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, U.K.
Ninian N LangBHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, U.K.
University of Glasgow · GBBlood Cancer UK · GBInstitute of Infection and Immunity · CAWestern General Hospital · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ageing is a major risk factor for the development of cardiovascular disease (CVD) and cancer. Whilst the cumulative effect of exposure to conventional cardiovascular risk factors is important, recent evidence highlights clonal haematopoiesis of indeterminant potential (CHIP) as a further key risk factor. CHIP reflects the accumulation of somatic, potentially pro-leukaemic gene mutations within haematopoietic stem cells over time. The most common mutations associated with CHIP and CVD occur in genes that also play central roles in the regulation of inflammation. While CHIP carriers have a low risk of haematological malignant transformation (<1% per year), their relative risk of mortality is increased by 40% and this reflects an excess of cardiovascular events. Evidence linking CHIP, inflammation and atherosclerotic disease has recently become better defined. However, there is a paucity of information about the role of CHIP in the development and progression of heart failure, particularly heart failure with preserved ejection fraction (HFpEF). While systemic inflammation plays a role in the pathophysiology of both heart failure with reduced and preserved ejection fraction (EF), it may be of greater relevance in the pathophysiology of HFpEF, which is also strongly associated with ageing. This review describes CHIP and its pathogenetic links with ageing, inflammation and CVD, while providing insight into its putative role in HFpEF.

Indexed as

Cardiovascular DiseasesClonal HematopoiesisHeart FailureInflammationAgingHumansRisk FactorsStroke Volumeageingatherosclerosiscardiovascular diseaseclonal haematopoiesis of indeterminate potentialheart failure

Identifiers

PMID33861346
PMCPMC8055963
OpenAlexW3153550493

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.