Evidence map›Paper›PMID 33001865›Full record

ArticleJCI insight2020

PDGFRA in vascular adventitial MSCs promotes neointima formation in arteriovenous fistula in chronic kidney disease.

Ke Song, Ying Qing, Qunying Guo, Eric K Peden, Changyi Chen, William E Mitch, Luan Truong, Jizhong Cheng

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-weighted citation impact, top 6% 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

24 citing papers in PubMed, 36 citations in OpenAlex.

  1. The critical role of gut-brain signalling in eating behaviour and obesity.Nature reviews. Gastroenterology & hepatology · 2026
    Review
  2. Article
  3. Targeting C1q signaling in fibro-adipogenic progenitors prevents regenerative fibrosis of aged muscle.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  4. Article
  5. Article
  6. GDF15: An emerging disease target and biomarker of metabolic diseases.Journal of endocrinological investigation · 2025
    Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. The Role of Gli1Biomolecules · 2023
    Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. 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

8 authors at 3 institutions in 2 countries.

Ke SongDepartment of Stomatology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Ying QingSelzman Institute for Kidney Health, Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Qunying GuoSelzman Institute for Kidney Health, Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Eric K PedenDepartment of Vascular Surgery, DeBakey Heart and Vascular Institute, Houston Methodist Hospital, Houston, Texas, USA.
Changyi ChenMichael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, Texas, USA.
William E MitchSelzman Institute for Kidney Health, Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Luan TruongDepartment of Pathology and Genomic Medicine, Houston Methodist Hospital, Houston, Texas, USA.
Jizhong ChengSelzman Institute for Kidney Health, Section of Nephrology, Department of Medicine, Baylor College of Medicine, Houston, Texas, USA.
Baylor College of Medicine · USHouston Methodist · USMethodist Hospital · US

Funding

CHRONIC KIDNEY DISEASE ADVERSELY INFLUENCES VASCULAR FUNCTIONSR01DK095867 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHENG, JIZHONG · 2013 to 2017
$1.7M
Interplay between skeletal muscle catabolism and remodeling of arteriovenous fistulae via YAP1/TAZ signalingR01DK124259 · NIDDK · BAYLOR COLLEGE OF MEDICINE · PI CHENG, JIZHONG · 2020 to 2023
$1.6M
NIDDK NIH HHS R01 DK095867NIDDK NIH HHS R01 DK124259
6 · The paper itself

Abstract

Chronic kidney disease (CKD) induces the failure of arteriovenous fistulas (AVFs) and promotes the differentiation of vascular adventitial GLI1-positive mesenchymal stem cells (GMCs). However, the roles of GMCs in forming neointima in AVFs remain unknown. GMCs isolated from CKD mice showed increased potential capacity of differentiation into myofibroblast-like cells. Increased activation of expression of PDGFRA and hedgehog (HH) signaling were detected in adventitial cells of AVFs from patients with end-stage kidney disease and CKD mice. PDGFRA was translocated and accumulated in early endosome when sonic hedgehog was overexpressed. In endosome, PDGFRA-mediated activation of TGFB1/SMAD signaling promoted the differentiation of GMCs into myofibroblasts, extracellular matrix deposition, and vascular fibrosis. These responses resulted in neointima formation and AVF failure. KO of Pdgfra or inhibition of HH signaling in GMCs suppressed the differentiation of GMCs into myofibroblasts. In vivo, specific KO of Pdgfra inhibited GMC activation and vascular fibrosis, resulting in suppression of neointima formation and improvement of AVF patency despite CKD. Our findings could yield strategies for maintaining AVF functions.

Indexed as

AnimalsArteriovenous FistulaCell DifferentiationMesenchymal Stem CellsMiceMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyofibroblastsNeointimaReceptor, Platelet-Derived Growth Factor alphaRenal Insufficiency, ChronicReceptor, Platelet-Derived Growth Factor alphaChronic kidney diseaseMouse stem cellsNephrologySignal transductionStem cells

Identifiers

PMID33001865
PMCPMC7710276
OpenAlexW3090285909

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.