Evidence map›Paper›PMID 37225873›Full record

ReviewNature reviews. Cardiology2023

Flow-induced reprogramming of endothelial cells in atherosclerosis.

Ian A Tamargo, Kyung In Baek, Yerin Kim, Christian Park, Hanjoong Jo

Open access · hybridAbstract readReview
In one paragraph

Review in Nature reviews. Cardiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 165 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
165citing papers in PubMed, 1 pooled it
34.2field-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

165 citing papers in PubMed, 1 synthesis or guideline pooled it, 222 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Review
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Early atherogenesis: In search of etiology.International journal of cardiology. Cardiovascular risk and prevention · 2026
    Review
  10. Nanomaterials-Based Immunotherapy for Atherosclerosis.Small (Weinheim an der Bergstrasse, Germany) · 2026
    Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
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  19. Review
  20. 4D force patterning enables spatial control of angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article

105 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

5 authors at 1 institution in 1 country.

Ian A Tamargo *Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
Kyung In Baek *Wallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
Yerin KimWallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
Christian ParkWallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA.
Hanjoong JoWallace H. Coulter Department of Biomedical Engineering, Emory University and Georgia Institute of Technology, Atlanta, GA, USA. hjo@emory.edu.ORCID 0000-0003-1833-372X
Georgia Institute of Technology · US

Funding

Research Trainng in Academic CardiologyT32HL007745 · NHLBI · EMORY UNIVERSITY · PI TAYLOR, WILLIAM ROBERT · 1994 to 2023
$10.6M
Shear stress, endothelial miRNAs, and AV calcificationR01HL119798 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG, YOGANATHAN, AJIT P · 2013 to 2022
$4.7M
Role of flow-sensitive KLK10 in endothelial dysfunction and atherosclerosisR01HL139757 · NHLBI · EMORY UNIVERSITY · PI JO, HANJOONG · 2018 to 2021
$1.6M
Integration of advanced imaging and multiOMICs to elucidate pro-atherogenic effects of endothelial-to-Immune cell-like transition (EndICLT)F32HL167625 · NHLBI · EMORY UNIVERSITY · PI BAEK, KYUNG IN · 2023 to 2023
$74k
NHLBI NIH HHS 5F31HL149285-03NHLBI NIH HHS F32 HL167625NHLBI NIH HHS HL151358NHLBI NIH HHS R01 HL119798NHLBI NIH HHS R01 HL139757NHLBI NIH HHS T32 HL007745
6 · The paper itself

Abstract

Atherosclerotic diseases such as myocardial infarction, ischaemic stroke and peripheral artery disease continue to be leading causes of death worldwide despite the success of treatments with cholesterol-lowering drugs and drug-eluting stents, raising the need to identify additional therapeutic targets. Interestingly, atherosclerosis preferentially develops in curved and branching arterial regions, where endothelial cells are exposed to disturbed blood flow with characteristic low-magnitude oscillatory shear stress. By contrast, straight arterial regions exposed to stable flow, which is associated with high-magnitude, unidirectional shear stress, are relatively well protected from the disease through shear-dependent, atheroprotective endothelial cell responses. Flow potently regulates structural, functional, transcriptomic, epigenomic and metabolic changes in endothelial cells through mechanosensors and mechanosignal transduction pathways. A study using single-cell RNA sequencing and chromatin accessibility analysis in a mouse model of flow-induced atherosclerosis demonstrated that disturbed flow reprogrammes arterial endothelial cells in situ from healthy phenotypes to diseased ones characterized by endothelial inflammation, endothelial-to-mesenchymal transition, endothelial-to-immune cell-like transition and metabolic changes. In this Review, we discuss this emerging concept of disturbed-flow-induced reprogramming of endothelial cells (FIRE) as a potential pro-atherogenic mechanism. Defining the flow-induced mechanisms through which endothelial cells are reprogrammed to promote atherosclerosis is a crucial area of research that could lead to the identification of novel therapeutic targets to combat the high prevalence of atherosclerotic disease.

Indexed as

AtherosclerosisEndothelial CellsAnimalsCellular ReprogrammingHumansStress, Mechanical

Identifiers

PMID37225873
PMCPMC10206587
OpenAlexW4377989539

What OpenQuestion holds

Textmetadata
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.