Evidence map›Paper›PMID 40207366›Full record

ReviewArteriosclerosis, thrombosis, and vascular biology2025

Fluid Shear Stress-Regulated Vascular Remodeling: Past, Present, and Future.

Hanqiang Deng, Anne Eichmann, Martin A Schwartz

Abstract readReview
In one paragraph

Review in Arteriosclerosis, thrombosis, and vascular biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing 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

26 citing papers in PubMed.

  1. Article
  2. Article
  3. Review
  4. Cerebral arteries in mice with sickle cell disease are exposed to larger areas of low wall shear stress.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  5. mBiomolecules · 2026
    Review
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  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
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  15. Review
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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

3 authors.

Hanqiang DengYale Cardiovascular Research Center CT (H.D., A.E., M.A.S.), Yale University School of Medicine, New Haven, CT.ORCID 0000-0001-5976-517X
Anne EichmannYale Cardiovascular Research Center CT (H.D., A.E., M.A.S.), Yale University School of Medicine, New Haven, CT.ORCID 0000-0001-5563-210X
Martin A SchwartzYale Cardiovascular Research Center CT (H.D., A.E., M.A.S.), Yale University School of Medicine, New Haven, CT.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
Flow regulation of the Alk1/Eng pathway in vascular homeostasis and diseaseR01HL169510 · NHLBI · YALE UNIVERSITY · PI Anne Christine Eichmann, Martin A Schwartz · 2023 to 2026
$3.0M
NHLBI NIH HHS R01 HL135582NHLBI NIH HHS R01 HL169510
6 · The paper itself

Abstract

The vascular system remodels throughout life to ensure adequate perfusion of tissues as they grow, regress, or change metabolic activity. Angiogenesis, the sprouting of new blood vessels to expand the capillary network, versus regression, in which endothelial cells die or migrate away to remove unneeded capillaries, controls capillary density. In addition, upstream arteries adjust their diameters to optimize blood flow to downstream vascular beds, which is controlled primarily by vascular endothelial cells sensing fluid shear stress (FSS) from blood flow. Changes in capillary density and small artery tone lead to changes in the resistance of the vascular bed, which leads to changes in flow through the arteries that feed these small vessels. The resultant decreases or increases in FSS through these vessels then stimulate their inward or outward remodeling, respectively. This review summarizes our knowledge of endothelial FSS-dependent vascular remodeling, offering insights into potential therapeutic interventions. We first provide a historical overview, then discuss the concept of set point and mechanisms of low-FSS-mediated and high-FSS-mediated inward and outward remodeling. We then cover in vivo animal models, molecular mechanisms, and clinical implications. Understanding the mechanisms underlying physiological endothelial FSS-mediated vascular remodeling and their failure due to mutations or chronic inflammatory and metabolic stresses may lead to new therapeutic strategies to prevent or treat vascular diseases.

Indexed as

Endothelial CellsHemodynamicsMechanotransduction, CellularVascular RemodelingAnimalsEndothelium, VascularHumansNeovascularization, PhysiologicRegional Blood FlowStress, Mechanicalcapillariescardiovascular diseasesendothelial cellsmutationvascular remodeling

Identifiers

PMID40207366
PMCPMC12094896

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.