Evidence map›Paper›PMID 25614287›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2015

Impaired integrin β3 delays endothelial cell regeneration and contributes to arteriovenous graft failure in mice.

Ming Liang, Yun Wang, Anlin Liang, Jin-Fei Dong, Jie Du, Jizhong Cheng

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 28% 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

10 citing papers in PubMed, 10 citations in OpenAlex.

  1. Transforming Growth Factors in Venous Thrombus Formation and Resolution.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  2. Article
  3. Challenges and strategies forBioactive materials · 2021
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Inflammation in Vein Graft Disease.Frontiers in cardiovascular medicine · 2018
    Review
  9. Review
  10. 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

6 authors at 3 institutions in 2 countries.

Ming LiangFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.).
Yun WangFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.).
Anlin LiangFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.).
Jin-Fei DongFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.).
Jie DuFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.).
Jizhong ChengFrom the Department of Nephrology, Guangzhou First People's Hospital, Guangzhou Medical University, Guangzhou, China (M.L.); Department of Cell Biology, Third Military Medical University, Chongqing, China (Y.W.); Puget Sound Blood Research Institute, Hematology Division, Department of Medicine, University of Washington, Seattle (J.-F.D.); Beijing Anzhen Hospital Affiliated to the Capital Medical University, Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing, China (J.D.); and Nephrology Division, Baylor College of Medicine, Houston, TX (M.L., Y.W., A.L., J.C.). jizhongc@bcm.edu.
Army Medical University · CNGuangzhou Medical University · CNGuangzhou First People's Hospital · CN

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI DAVID R ROWLEY · 2007 to 2026
$73.9M
Virology CoreP30AI036211 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BUTEL, JANET S · 1994 to 2015
$21.7M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR01DK037175 · NIDDK · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI Zhaoyong Hu · 1986 to 2026
$4.3M
PROTEIN NUTRITION IN EXPERIMENTAL UREMIAR37DK037175 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI MITCH, WILLIAM EVANS · 2006 to 2015
$3.8M
CHRONIC KIDNEY DISEASE ADVERSELY INFLUENCES VASCULAR FUNCTIONSR01DK095867 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHENG, JIZHONG · 2013 to 2017
$1.7M
BD Biosciences Special Order LSRIIS10RR024574 · NCRR · BAYLOR COLLEGE OF MEDICINE · PI LUMPKIN, ELLEN A · 2009 to 2009
$430k
NCI NIH HHS P30 CA125123NCI NIH HHS P30CA125123NCRR NIH HHS S10 RR024574NCRR NIH HHS S10RR024574NIAID NIH HHS P30 AI036211NIAID NIH HHS P30AI036211NIDDK NIH HHS R01 DK037175NIDDK NIH HHS R01 DK095867NIDDK NIH HHS R37 DK037175
6 · The paper itself

Abstract

objectiveNeointima formation is associated with stenosis and subsequent thrombosis in arteriovenous grafts (AVGs). A role of integrin β3 in the neointima formation of AVGs remains poorly understood. APPROACH AND

resultsIn integrin β3(-/-) mice, we found significantly accelerated occlusion of AVGs compared with the wild-type mice. This is caused by the development of neointima and lack of endothelial regeneration. The latter is a direct consequence of impaired functions of circulating angiogenic cells (CACs) and platelets in integrin β3(-/-) mice. Evidence suggests the involvement of platelet regulating CAC homing to and differentiation at graft sites via transforming growth factor-β1 and Notch signaling pathway. First, CACs deficient of integrin β3 impaired adhesion activity toward exposed subendothelium. Second, platelets from integrin β3(-/-) mice failed to sufficiently stimulate CACs to differentiate into mature endothelial cells. Finally, we found that transforming growth factor-β1 level was increased in platelets from integrin β3(-/-) mice and resulted in enhanced Notch1 activation in CACs in AVGs. These results demonstrate that integrin β3 is critical for endothelial cell homing and differentiation. The increased transforming growth factor-β1 and Notch1 signaling mediates integrin β3(-/-)-induced AVG occlusion. This accelerated occlusion of AVGs was reversed in integrin β3(-/-) mice transplanted with the bone marrow from wild-type mice.

conclusionsOur results suggest that boosting integrin β3 function in the endothelial cells and platelets could prevent neointima and thrombosis in AVGs.

Indexed as

Cell ProliferationRegenerationAnimalsArteriovenous Shunt, SurgicalBlood PlateletsBone Marrow TransplantationCarotid Artery, CommonCell AdhesionCell DifferentiationCell MovementCells, CulturedCoculture TechniquesConstriction, PathologicDisease Models, AnimalEndothelial CellsGraft Occlusion, VascularIntegrin beta3Notch1 protein, mouseReceptor, Notch1Tgfb1 protein, mouseTransforming Growth Factor beta1arteriovenous graftcirculating angiogenic cellsintegrin β3neointima

Identifiers

PMID25614287
PMCPMC4671198
OpenAlexW2099400510

What OpenQuestion holds

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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 OpenQuestion graph.