Evidence map›Paper›PMID 28839221›Full record

ArticleScientific reports2017

Exosomes from high glucose-treated glomerular endothelial cells trigger the epithelial-mesenchymal transition and dysfunction of podocytes.

Xiaoming Wu, Yanbin Gao, Liping Xu, Wanyu Dang, Huimin Yan, Dawei Zou, Zhiyao Zhu, Liangtao Luo, Nianxiu Tian, Xiaolei Wang and 2 more

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

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed
8.1field-weighted citation impact, top 1% 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

121 citing papers in PubMed, 169 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. The role of extracellular vesicles in kidney disease progression.Kidney research and clinical practice · 2026
    Article
  14. Article
  15. Review
  16. The Life of a Kidney Podocyte.Acta physiologica (Oxford, England) · 2025
    Review
  17. Article
  18. Review
  19. Article
  20. Review

61 more citing papers are in PubMed but not listed here.

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

12 authors at 1 institution in 1 country.

Xiaoming WuBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Yanbin GaoBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China. dfyynfm@163.com.
Liping XuBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Wanyu DangBeijing Children's Hospital, Capital Medical University, NO. 56, Nanlishi Road, Xi Cheng District, Beijing, 100045, China.
Huimin YanBeijing Children's Hospital, Capital Medical University, NO. 56, Nanlishi Road, Xi Cheng District, Beijing, 100045, China.
Dawei ZouBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Zhiyao ZhuBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Liangtao LuoBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Nianxiu TianBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Xiaolei WangBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Yu TongBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Zheji HanBeijing Key Lab of TCM Collateral Disease Theory Research, School of Traditional Chinese Medicine, Capital Medical University, No.10, Youanmenwai, Xitoutiao, Fengtai District, Beijing, 100069, China.
Capital Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

New data indicate that abnormal glomerular endothelial cell (GEC)-podocyte crosstalk plays a critical role in diabetic nephropathy (DN). The aim of our study is to investigate the role of exosomes from high glucose (HG)-treated GECs in the epithelial-mesenchymal transition (EMT) and dysfunction of podocytes. In this study, exosomes were extracted from GEC culture supernatants and podocytes were incubated with the GEC-derived exosomes. Here, we demonstrate that HG induces the endothelial-mesenchymal transition (EndoMT) of GECs and HG-treated cells undergoing the EndoMT secrete more exosomes than normal glucose (NG)-treated GECs. We show that GEC-derived exosomes can be internalized by podocytes and exosomes from HG-treated cells undergoing an EndoMT-like process can trigger the podocyte EMT and barrier dysfunction. Our study reveals that TGF-β1 mRNA is enriched in exosomes from HG-treated GECs and probably mediates the EMT and dysfunction of podocytes. In addition, our experimental results illustrate that canonical Wnt/β-catenin signaling is involved in the exosome-induced podocyte EMT. Our findings suggest the importance of paracrine communication via exosomes between cells undergoing the EndoMT and podocytes for renal fibrosis in DN. Thus, protecting GECs from the EndoMT and inhibiting TGF-β1-containing exosomes release from GECs is necessary to manage renal fibrosis in DN.

Indexed as

Epithelial-Mesenchymal TransitionAnimalsBiomarkersCells, CulturedDiabetic NephropathiesEndocytosisEndothelial CellsExosomesGene ExpressionGlucoseKidney GlomerulusMicePermeabilityPhenotypePodocytesTransforming Growth Factor beta1BiomarkersGlucoseTransforming Growth Factor beta1

Identifiers

PMID28839221
PMCPMC5571220
OpenAlexW2749238253

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.