Evidence map›Paper›PMID 32735822›Full record

ReviewStem cell reports2020

Putative Mechanisms Underlying Cardiovascular Disease Associated with Clonal Hematopoiesis of Indeterminate Potential.

Sarah S Burns, Reuben Kapur

Open access · goldAbstract readReview
In one paragraph

Review in Stem cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 31% 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

6 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
  2. Article
  3. Science advances · 2025
    Article
  4. Article
  5. Review
  6. 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 1 institution in 1 country.

Sarah S BurnsDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA.
Reuben KapurDepartment of Medical and Molecular Genetics, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Pediatrics, Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, IN 46202, USA; Department of Molecular Biology and Biochemistry, Indiana University School of Medicine, Indianapolis, IN 46202, USA. Electronic address: rkapur@iupui.edu.
Indiana University – Purdue University Indianapolis · US

Funding

Role of p21 activated kinase in LeukemogenesisR01CA173852 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2014 to 2025
$3.4M
Role of Shp2 in FLT3-ITD-Induced LeukemogenesisR01CA134777 · NCI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2011 to 2023
$3.4M
Hyperglycemia mediated myeloproliferative diseaseR01HL140961 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.3M
Targeting Novel Pathways in JMMLR01HL146137 · NHLBI · INDIANA UNIVERSITY INDIANAPOLIS · PI KAPUR, REUBEN · 2019 to 2022
$2.2M
NCI NIH HHS R01 CA134777NCI NIH HHS R01 CA173852NHLBI NIH HHS R01 HL140961NHLBI NIH HHS R01 HL146137
6 · The paper itself

Abstract

Characterized by the expansion of somatic mutations in the hematopoietic lineages of aging individuals, clonal hematopoiesis of indeterminate potential (CHIP) is a common condition that increases the risk of developing hematological malignancies and cardiovascular disease (CVD). The presence of CHIP-associated mutations in hematopoietic stem and progenitor cells (HSPCs) suggests that these mutations may alter the functions of the diverse hematopoietic lineages, many of which influence the pathogenesis of CVD. Inflammation may be a potential pathogenic mechanism, linking both CVD and hematological malignancy. However, it remains unknown whether CHIP-associated CVD and hematological malignancy are features of a common disease spectrum. The contributions of CHIP-associated mutations to both CVD and hematological malignancy underscore the importance of stem cell biology in pathogenesis and treatment. This review discusses possible mechanisms underlying the contributions of multiple hematopoietic lineages to CHIP-associated CVD and the putative pathogenic links between CHIP-associated CVD and hematological malignancy.

Indexed as

Clonal HematopoiesisCardiovascular DiseasesCell LineageEpigenesis, GeneticHumansInflammationModels, Biologicalcardiovascular diseaseclonal hematopoiesis of indeterminate potentialhematological malignancyhematopoietic stem and progenitor cellsinflammation

Identifiers

PMID32735822
PMCPMC7419714
OpenAlexW3046582987

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.