Evidence map›Paper›PMID 26550455›Full record

ArticleAmerican journal of translational research2015

Low molecular weight fucoidan ameliorates diabetic nephropathy via inhibiting epithelial-mesenchymal transition and fibrotic processes.

Jihui Chen, Wentong Cui, Quanbin Zhang, Yingli Jia, Yi Sun, Lin Weng, Dali Luo, Hong Zhou, Baoxue Yang

Abstract read
In one paragraph

Article in American journal of translational research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.5field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 40 citations in OpenAlex.

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  11. Fucoidan fromMarine drugs · 2021
    Article
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  19. Fucoidans in Nanomedicine.Marine drugs · 2016
    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

9 authors at 1 institution in 1 country.

Jihui ChenState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China ; Department of Pharmacy, Xin-Hua Hospital Affiliated to Medical School, Shanghai Jiao Tong University Shanghai 200092, China.
Wentong CuiDepartment of Pharmacology, Capital Medical University Beijing 100069, China.
Quanbin ZhangInstitute of Oceanology, Chinese Academy of Sciences Qingdao 266071, China.
Yingli JiaState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China.
Yi SunState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China.
Lin WengState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China.
Dali LuoDepartment of Pharmacology, Capital Medical University Beijing 100069, China.
Hong ZhouState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China.
Baoxue YangState Key Laboratory of Natural and Biomimetic Drugs, Key Laboratory of Molecular Cardiovascular Sciences, Ministry of Education, and Department of Pharmacology, School of Basic Medical Sciences, Peking University Beijing 100191, China.
Chinese Academy of Sciences · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy (DN) is one of the most serious microvascular complications of diabetes and may lead to end-stage renal disease (ESRD) and chronic renal failure. The aim of this study was to determine whether low-molecular-weight fucoidan (LMWF) can reduce harmful transforming growth factor-β (TGF-β)-mediated renal fibrosis in DN using in vitro and in vivo experimental models. The experimental results showed that LMWF significantly reversed TGF-β1-induced epithelial-mesenchymal transition and dose-dependently inhibited accumulation of extracellular matrix proteins, including connective tissue growth factor and fibronectin. It was found that LMWF significantly reduced blood urea nitrogen and blood creatinine in both type 1 and type 2 diabetic rat models. H&E, PAS and Masson's trichrome staining of kidney tissue showed LMWF significantly reduced renal interstitial fibrosis. Treatment with LMWF significantly increased E-cadherin expression and reduced α-SMA, CTGF and fibronectin expression in both type 1 and type 2 diabetic models. LMWF also decreased the phosphorylation of Akt, ERK1/2, p38 and Smad3 in vitro and in vivo. These data suggest that LMWF may protect kidney from dysfunction and fibrogenesis by inhibiting TGF-β pathway and have the potential benefit to slow down the progression of DN.

Indexed as

diabetic nephropathyepithelialto-mesenchymal transitionextracellular matrixFucoidantransforming growth factor-β1tubulointerstitial fibrosis

Identifiers

PMID26550455
PMCPMC4626417
OpenAlexW2190837823

What OpenQuestion holds

Textmetadata
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.