Evidence map›Paper›PMID 39752487›Full record

ArticleScience advances2025

cSTAR analysis identifies endothelial cell cycle as a key regulator of flow-dependent artery remodeling.

Hanqiang Deng, Oleksii S Rukhlenko, Divyesh Joshi, Xiaoyue Hu, Philipp Junk, Anna Tuliakova, Boris N Kholodenko, Martin A Schwartz

Abstract read
In one paragraph

Article in Science advances, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
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

14 citing papers in PubMed.

  1. Polycomb Repressive Complex 2 drives flow-sensitive endothelial states underlying vascular inflammation and disease.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Fluid Shear Stress-Regulated Vascular Remodeling: Past, Present, and Future.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  10. SilencingInternational journal of molecular sciences · 2025
    Article
  11. Article
  12. Endothelial heterogeneity shapes shear stress response: a transcriptomic perspective.Research and practice in thrombosis and haemostasis · 2025
    Article
  13. Article
  14. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors.

Hanqiang DengYale Cardiovascular Research Center, Yale School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0001-5976-517X
Oleksii S RukhlenkoSystems Biology Ireland, School of Medicine, University College Dublin, Dublin, Ireland.ORCID 0000-0003-1863-4987
Divyesh JoshiYale Cardiovascular Research Center, Yale School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0002-4415-2677
Xiaoyue HuSection of Cardiovascular Medicine, Department of Internal Medicine, Yale School of Medicine, New Haven, CT 06511, USA.
Philipp JunkSystems Biology Ireland, School of Medicine, University College Dublin, Dublin, Ireland.ORCID 0000-0002-5228-3896
Anna TuliakovaSystems Biology Ireland, School of Medicine, University College Dublin, Dublin, Ireland.ORCID 0009-0006-3508-5085
Boris N KholodenkoSystems Biology Ireland, School of Medicine, University College Dublin, Dublin, Ireland.ORCID 0000-0002-9483-4975
Martin A SchwartzYale Cardiovascular Research Center, Yale School of Medicine, New Haven, CT 06511, USA.ORCID 0000-0002-2071-1243

Funding

Endothelial-to-mesenchyma transition and atherosclerosisR01HL135582 · NHLBI · YALE UNIVERSITY · PI SCHWARTZ, MARTIN A, SIMONS, MICHAEL · 2017 to 2024
$6.6M
Multiscale Modeling to Optimize Inhibition of Oncogenic ERK Pathway SignalingR01CA244660 · NCI · YALE UNIVERSITY · PI HLAVACEK, WILLIAM S, KHOLODENKO, BORIS N · 2020 to 2024
$3.4M
A QUANTITATIVE, PREDICTIVE MODEL OF VASCULAR REMODELING IN HEALTH AND DISEASER01HL171773 · NHLBI · YALE UNIVERSITY · PI Martin A Schwartz, Michael Simons · 2024 to 2026
$2.0M
NCI NIH HHS R01 CA244660NHLBI NIH HHS R01 HL135582NHLBI NIH HHS R01 HL171773
6 · The paper itself

Abstract

Fluid shear stress (FSS) from blood flow sensed by vascular endothelial cells (ECs) determines vessel behavior, but regulatory mechanisms are only partially understood. We used cell state transition assessment and regulation (cSTAR), a powerful computational method, to elucidate EC transcriptomic states under low shear stress (LSS), physiological shear stress (PSS), high shear stress (HSS), and oscillatory shear stress (OSS) that induce vessel inward remodeling, stabilization, outward remodeling, or disease susceptibility, respectively. Combined with a publicly available database on EC transcriptomic responses to drug treatments, this approach inferred a regulatory network controlling EC states and made several notable predictions. Particularly, inhibiting cell cycle-dependent kinase (CDK) 2 was predicted to initiate inward remodeling and promote atherogenesis. In vitro, PSS activated CDK2 and induced late G

Indexed as

Cell CycleCyclin-Dependent Kinase 2Endothelial CellsStress, MechanicalVascular RemodelingAnimalsArteriesAtherosclerosisGene Expression ProfilingHumansMiceTranscriptomeCdk2 protein, mouseCyclin-Dependent Kinase 2

Identifiers

PMID39752487
PMCPMC11698091

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.