Evidence map›Paper›PMID 29209018›Full record

ArticleScientific reports2017

Novel Mechanism of the Pericyte-Myofibroblast Transition in Renal Interstitial Fibrosis: Core Fucosylation Regulation.

Nan Wang, Yiyao Deng, Anqi Liu, Nan Shen, Weidong Wang, Xiangning Du, Qingzhu Tang, Shuangxin Li, Zach Odeh, Taihua Wu and 1 more

Open access · goldAbstract read
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 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

46 citing papers in PubMed, 68 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Glycosylation in kidney diseases.Precision clinical medicine · 2025
    Review
  7. Review
  8. Review
  9. Fibroblast Heterogeneity in Inflammatory Bowel Disease.International journal of molecular sciences · 2024
    Review
  10. Article
  11. Article
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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

11 authors at 1 institution in 1 country.

Nan WangDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.ORCID 0000-0002-9589-1621
Yiyao DengDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Anqi LiuDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Nan ShenDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Weidong WangDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Xiangning DuDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Qingzhu TangDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Shuangxin LiDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Zach OdehDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China.
Taihua WuDepartments of Respiratory Medicine, The First Affiliated Hospital of Dalian Medical University, 222# Zhongshan Road, No. 222 Zhongshan Road, Dalian, 116011, China. wutaihuadoc@126.com.
Hongli LinDepartment of Nephrology, The First Affiliated Hospital of Dalian Medical University, Key Laboratory of Kidney Disease of Liaoning Province, The Center for the Transformation Medicine of Kidney Disease of Liaoning Province, No. 222 Zhongshan Road, Dalian, 116011, China. linhongli@vip.163.com.
Dalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Pericytes have been identified as a major source of myofibroblasts in renal interstitial fibrosis (RIF). The overactivation of several signaling pathways, mainly the TGF-β and PDGF pathways, initiates the pericyte-myofibroblast transition during RIF. Key receptors in these two pathways have been shown to be modified by fucosyltransferase 8 (FUT8), the enzyme that catalyzes core fucosylation. This study postulated that core fucosylation might play an important role in regulating the pericyte transition in RIF. The data showed that core fucosylation increased with the extent of RIF in patients with IgA nephropathy (IgAN). Similarly, core fucosylation of pericytes increased in both a unilateral ureteral occlusion (UUO) mouse model and an in vitro model of pericyte transition. Inhibition of core fucosylation by adenoviral-mediated FUT8 shRNA in vivo and FUT8 siRNA in vitro significantly reduced pericyte transition and RIF. In addition, the activation of both the TGF-β/Smad and PDGF/ERK pathways was blocked by core fucosylation inhibition. In conclusion, core fucosylation may regulate the pericyte transition in RIF by modifying both the TGF-β/Smad and PDGF/ERK pathways. Glycosylation might be a novel "hub" target to prevent RIF.

Indexed as

AdultAnimalsDisease Models, AnimalFemaleFibrosisFucosyltransferasesGlomerulonephritis, IGAGlycosylationHumansKidneyKidney DiseasesMaleMice, Inbred C57BLMiddle AgedMyofibroblastsPericytesFucosyltransferasesGlycoprotein 6-alpha-L-fucosyltransferasePlatelet-Derived Growth FactorReceptors, Transforming Growth Factor beta

Identifiers

PMID29209018
PMCPMC5717002
OpenAlexW2769288944

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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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.