Evidence mapPaperPMID 35510552Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2022

Endothelial Cell TGF-β (Transforming Growth Factor-Beta) Signaling Regulates Venous Adaptive Remodeling to Improve Arteriovenous Fistula Patency.

Ryosuke Taniguchi, Yuichi Ohashi, Jung Seok Lee, Haidi Hu, Luis Gonzalez, Weichang Zhang, John Langford, Yutaka Matsubara, Bogdan Yatsula, George Tellides and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.7field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 28 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Observational
  5. Article
  6. Sustained tenascin-C expression drives neointimal hyperplasia and promotes aortocaval fistula failure.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  7. Review
  8. Article
  9. Nanomedicine for Diagnosis and Treatment of Cardiac Fibrosis.International journal of nanomedicine · 2025
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. The rodent models of arteriovenous fistula.Frontiers in cardiovascular medicine · 2024
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 3 institutions in 3 countries.

Ryosuke TaniguchiVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.ORCID 0000-0001-7226-1363
Yuichi OhashiVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.
Jung Seok LeeDepartment of Biomedical Engineering, Yale University, New Haven, CT (J.S.L., T.M.F.).ORCID 0000-0002-9810-8647
Haidi HuVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.
Luis GonzalezVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.ORCID 0000-0003-2877-7287
Weichang ZhangVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.
John LangfordVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.ORCID 0000-0002-7307-8664
Yutaka MatsubaraVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.ORCID 0000-0002-9187-8403
Bogdan YatsulaVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.
George TellidesVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.
Tarek M FahmyDepartment of Biomedical Engineering, Yale University, New Haven, CT (J.S.L., T.M.F.).
Katsuyuki HoshinaDivision of Vascular Surgery, The University of Tokyo, Japan (R.T., Y.O., K.H.).ORCID 0000-0001-8526-968X
Alan DardikVascular Biology and Therapeutics Program (R.T., Y.O., H.H., L.G., W.Z., J.L., Y.M., B.Y., G.T., A.D.), Yale School of Medicine, New Haven, CT.ORCID 0000-0001-5022-7367
Yale University · USKyushu University · JPYKK (Japan) · JP

Funding

Manipulating the matrix to improve arteriovenous fistula patencyR01HL144476 · YALE UNIVERSITY · 2025 to 2025
$758k
NHLBI NIH HHS R01 HL128406NHLBI NIH HHS R01 HL144476
6 · The paper itself

Abstract

backgroundArteriovenous fistulae (AVF) are the gold standard for vascular access for hemodialysis. Although the vein must thicken and dilate for successful hemodialysis, excessive wall thickness leads to stenosis causing AVF failure. Since TGF-β (transforming growth factor-beta) regulates ECM (extracellular matrix) deposition and smooth muscle cell (SMC) proliferation-critical components of wall thickness-we hypothesized that disruption of TGF-β signaling prevents excessive wall thickening during venous remodeling.

methodsA mouse aortocaval fistula model was used. SB431542-an inhibitor of TGF-β receptor I-was encapsulated in nanoparticles and applied to the AVF adventitia in C57BL/6J mice. Alternatively, AVFs were created in mice with conditional disruption of TGF-β receptors in either SMCs or endothelial cells. Doppler ultrasound was performed serially to confirm patency and to measure vessel diameters. AVFs were harvested at predetermined time points for histological and immunofluorescence analyses.

resultsInhibition of TGF-β signaling with SB431542-containing nanoparticles significantly reduced p-Smad2-positive cells in the AVF wall during the early maturation phase (days 7-21) and was associated with decreased AVF wall thickness that showed both decreased collagen density and decreased SMC proliferation. SMC-specific TGF-β signaling disruption decreased collagen density but not SMC proliferation or wall thickness. Endothelial cell-specific TGF-β signaling disruption decreased both collagen density and SMC proliferation in the AVF wall and was associated with reduced wall thickness, increased outward remodeling, and improved AVF patency.

conclusionsEndothelial cell-targeted TGF-β inhibition may be a translational strategy to improve AVF patency.

Indexed as

Arteriovenous FistulaArteriovenous Shunt, SurgicalAnimalsCollagenDisease Models, AnimalEndothelial CellsMiceMice, Inbred C57BLTransforming Growth Factor betaTransforming Growth FactorsVascular RemodelingCollagenTransforming Growth Factor betaTransforming Growth Factorsarteriovenous fistulaendothelial cellsextracellular matrixmyocytes, smooth muscletransforming growth factor-beta

Identifiers

PMID35510552
PMCPMC9233042
OpenAlexW4229004167

What Socratic holds

Textmetadata
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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.