Evidence map›Paper›PMID 35445383›Full record

ReviewThrombosis and haemostasis2022

Hematopoiesis of Indeterminate Potential and Atherothrombotic Risk.

Andrew J Murphy, Dragana Dragoljevic, Pradeep Natarajan, Nan Wang

Open access · hybridAbstract readReview
In one paragraph

Review in Thrombosis and haemostasis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
0.5field-weighted citation impact, top 37% 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

0 citing papers in PubMed, 3 citations in OpenAlex.

No citing paper in PubMed yet.

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

4 authors at 3 institutions in 2 countries.

Andrew J MurphyHaematopoiesis and Leukocyte Biology, Baker Heart and Diabetes Institute, Melbourne, Australia.
Dragana DragoljevicHaematopoiesis and Leukocyte Biology, Baker Heart and Diabetes Institute, Melbourne, Australia.
Pradeep NatarajanCardiology Division, Department of Medicine, Cardiovascular Research Center, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts, United States.
Nan WangDivision of Molecular Medicine, Department of Medicine, Columbia University Medical Center, New York, United States.
Baker Heart and Diabetes Institute · AUColumbia University Irving Medical Center · USMassachusetts General Hospital · US

Funding

Clonal hematopoiesis in humans: determinants of development and progressionR01HL148050 · NHLBI · BAYLOR COLLEGE OF MEDICINE · PI BALLANTYNE, CHRISTIE MITCHELL, NATARAJAN, PRADEEP · 2019 to 2022
$5.9M
APP1142938 National Health and Medical Research CouncilAPP1194329 National Health and Medical Research CouncilNHLBI NIH HHS R01 HL148050R01DK125782 National Institute of Diabetes and Digestive and Kidney DiseasesR01HL118567 National Heart, Lung, and Blood InstituteR01HL127564 National Heart, Lung, and Blood InstituteR01HL135242 National Heart, Lung, and Blood InstituteR01HL142711 National Heart, Lung, and Blood InstituteR01HL148050 National Heart, Lung, and Blood InstituteR01HL148071 National Heart, Lung, and Blood InstituteR01HL148565 National Heart, Lung, and Blood InstituteR01HL151152 National Heart, Lung, and Blood InstituteR01HL151283 National Heart, Lung, and Blood InstituteTNE-18CVD04 Fondation Leducq
6 · The paper itself

Abstract

Hematopoiesis is the process of blood production, essential for the continued supply of immune cells and red blood cells. However, the proliferative nature of hematopoietic stem cells (HSCs) renders them susceptible to developing somatic mutations. HSCs carrying a mutation can gain a selective advantage over normal HSCs and result in hematological disorders. One such disorder is termed clonal hematopoiesis of indeterminate potential (CHIP), a premalignant state associated with aging, where the mutant HSCs are responsible for producing a small portion of mature immune cells in the circulation and subsequently in tissues. People with CHIP have been shown to have an increased risk of mortality due to cardiovascular disease (CVD). Why this occurs is under rigorous investigation, but the majority of the studies to date have suggested that increased atherosclerosis is due to heightened inflammatory cytokine release from mutant lesional macrophages. However, given CHIP is driven by several mutations, other hematopoietic lineages can be altered to promote CVD. In this review we explore the relationship between mutations in genes causing CHIP and atherothrombotic disorders, along with potential mechanisms of enhanced clonal outgrowth and potential therapies and strategies to slow CHIP progression.

Indexed as

AtherosclerosisCardiovascular DiseasesHematopoiesisHematopoietic Stem CellsHumansMutation

Identifiers

PMID35445383
PMCPMC9420552
OpenAlexW4224262469

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.