Evidence map›Paper›PMID 21998146›Full record

ArticleMolecular endocrinology (Baltimore, Md.)2011

Sphingosine kinase-1 pathway mediates high glucose-induced fibronectin expression in glomerular mesangial cells.

Tian Lan, Weihua Liu, Xi Xie, Suowen Xu, Kaipeng Huang, Jing Peng, Xiaoyan Shen, Peiqing Liu, Lijing Wang, Pu Xia and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular endocrinology (Baltimore, Md.), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

25 citing papers in PubMed, 67 citations in OpenAlex.

  1. Review
  2. Article
  3. The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  4. Review
  5. Article
  6. Implications of Sphingolipid Metabolites in Kidney Diseases.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Sphingosine-1-phosphate pathway in renal fibrosis.American journal of physiology. Renal physiology · 2018
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. 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 3 institutions in 2 countries.

Tian LanLaboratory of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-sen University, Guangdong Pharmaceutical University, Guangzhou 510006, China.
Weihua Liu
Xi Xie
Suowen Xu
Kaipeng Huang
Jing Peng
Xiaoyan Shen
Peiqing Liu
Lijing Wang
Pu Xia
Heqing Huang
Guangdong Pharmaceutical University · CNCentenary Institute · AUSecond Affiliated Hospital of Guangzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Diabetic nephropathy is characterized by accumulation of glomerular extracellular matrix proteins, such as fibronectin (FN). Here, we investigated whether sphingosine kinase (SphK)1 pathway is responsible for the elevated FN expression in diabetic nephropathy. The SphK1 pathway and FN expression were examined in streptozotocin-induced diabetic rat kidney and glomerular mesangial cells (GMC) exposed to high glucose (HG). FN up-regulation was concomitant with activation of the SphK1 pathway as reflected in an increase in the expression and activity of SphK1 and sphingosine 1-phosphate (S1P) production in both diabetic kidney and HG-treated GMC. Overexpression of wild-type SphK1 (SphK(WT)) significantly induced FN expression, whereas treatment with a SphK inhibitor, N,N-dimethylsphingosine, or transfection of SphK1 small interference RNA or dominant-negative SphK1 (SphK(G82D)) abolished HG-induced FN expression. Furthermore, addition of exogenous S1P significantly induced FN expression in GMC with an induction of activator protein 1 (AP-1) activity. Inhibition of AP-1 activity by curcumin attenuated the S1P-induced FN expression. Finally, by inhibiting SphK1 activity, both N,N-dimethylsphingosine and SphK(G82D) markedly attenuated the HG-induced AP-1 activity. Taken together, these results demonstrated that the SphK1 pathway plays a critical role in matrix accumulation in GMC under diabetic condition, suggesting that the SphK1 pathway could be a potential therapeutic target for diabetic nephropathy.

Indexed as

AnimalsBlood GlucoseCells, CulturedDiabetes Mellitus, ExperimentalDiabetic NephropathiesExtracellular MatrixFibronectinsGene ExpressionGene Knockdown TechniquesGlucoseKidney GlomerulusLysophospholipidsMaleMesangial CellsPhosphotransferases (Alcohol Group Acceptor)ProteinuriaBlood GlucoseFibronectinsGlucoseLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)Reactive Oxygen SpeciesReceptors, LysosphingolipidSphingosinesphingosine 1-phosphateSphingosine KinaseTranscription Factor AP-1

Identifiers

PMID21998146
PMCPMC3231833
OpenAlexW2036088171

What OpenQuestion holds

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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.