Evidence map›Paper›PMID 36049115›Full record

ReviewPhysiological reviews2023

Clonal hematopoiesis, somatic mosaicism, and age-associated disease.

Megan A Evans, Kenneth Walsh

Open access · greenAbstract readReview
In one paragraph

Review in Physiological reviews, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
12.3field-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

75 citing papers in PubMed, 86 citations in OpenAlex.

  1. Review
  2. Exacerbation of inflammatory bone loss in TET2-driven clonal hematopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Article
  3. Article
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  5. Risk factors of clonal hematopoiesis of indeterminate potential.Clinical medicine (London, England) · 2026
    Article
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  19. Review
  20. Review

15 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Megan A EvansHematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, Virginia.
Kenneth WalshHematovascular Biology Center, Robert M. Berne Cardiovascular Research Center, University of Virginia School of Medicine, Charlottesville, Virginia.ORCID 0000-0001-7580-2276
University of Virginia · US

Funding

Clonal hematopoiesis and accelerated metabolic dysfunction in obesityR01HL139819 · NHLBI · UNIVERSITY OF VIRGINIA · PI WALSH, KENNETH · 2019 to 2022
$2.1M
Hematopoietic stem cell mutations and ischemic cardio-metabolic diseaseR01HL141256 · NHLBI · UNIVERSITY OF VIRGINIA · PI WALSH, KENNETH · 2019 to 2022
$1.9M
Clonal hematopoiesis and severity of COVID-19 diseaseR21AG072095 · NIA · UNIVERSITY OF VIRGINIA · PI DEFILIPPI, CHRISTOPHER R, WALSH, KENNETH · 2021 to 2022
$457k
HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL139819HHS | NIH | National Heart, Lung, and Blood Institute (NHLBI) HL141256HHS | NIH | National Institute on Aging (NIA) AG072095NHLBI NIH HHS R01 HL139819NHLBI NIH HHS R01 HL141256NIA NIH HHS R21 AG072095
6 · The paper itself

Abstract

Somatic mosaicism, the occurrence of multiple genetically distinct cell clones within the same tissue, is an evitable consequence of human aging. The hematopoietic system is no exception to this, where studies have revealed the presence of expanded blood cell clones carrying mutations in preleukemic driver genes and/or genetic alterations in chromosomes. This phenomenon is referred to as clonal hematopoiesis and is remarkably prevalent in elderly individuals. While clonal hematopoiesis represents an early step toward a hematological malignancy, most individuals will never develop blood cancer. Somewhat unexpectedly, epidemiological studies have found that clonal hematopoiesis is associated with an increase in the risk of all-cause mortality and age-related disease, particularly in the cardiovascular system. Studies using murine models of clonal hematopoiesis have begun to shed light on this relationship, suggesting that driver mutations in mature blood cells can causally contribute to aging and disease by augmenting inflammatory processes. Here we provide an up-to-date review of clonal hematopoiesis within the context of somatic mosaicism and aging and describe recent epidemiological studies that have reported associations with age-related disease. We will also discuss the experimental studies that have provided important mechanistic insight into how driver mutations promote age-related disease and how this knowledge could be leveraged to treat individuals with clonal hematopoiesis.

Indexed as

Cardiovascular DiseasesHematopoiesisAgedAnimalsClonal HematopoiesisHematopoietic Stem CellsHumansMiceMosaicismMutationage-related clonal hematopoiesisclonal hematopoiesis of indeterminate potential (CHIP)inflammagingmosaic chromosomal alterationstherapy-related clonal hematopoiesis

Identifiers

PMID36049115
PMCPMC9639777
OpenAlexW4294202978

What OpenQuestion holds

Textmetadata
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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.