Evidence map›Paper›PMID 22904348›Full record

ArticleJournal of the American Society of Nephrology : JASN2012

Tuberin inhibits production of the matrix protein fibronectin in diabetes.

Samy L Habib, Mukesh Yadav, Shaza Tizani, Basant Bhandari, Anthony J Valente

Open access · bronzeAbstract read
In one paragraph

Article in Journal of the American Society of Nephrology : JASN, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

13 citing papers in PubMed, 22 citations in OpenAlex.

  1. Galectin-1 is a new fibrosis protein in type 1 and type 2 diabetes.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    Article
  2. Article
  3. Evaluation of mTOR signaling pathway proteins in rat gastric mucosa exposed to sulfite and ghrelin.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2018
    Article
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  5. Article
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  10. The role of microRNAs in diabetic nephropathy.Journal of diabetes research · 2014
    Review
  11. Tuberin in renal cell hypertrophy.Cell cycle (Georgetown, Tex.) · 2014
    Article
  12. Rheb/mTORC1 signaling promotes kidney fibroblast activation and fibrosis.Journal of the American Society of Nephrology : JASN · 2013
    Article
  13. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Samy L HabibDepartment of Cellular and Structural Biology, The University of Texas Health Science Center, 7703 Floyd Curl Drive, San Antonio, TX 78229, USA. habib@uthscsa.edu
Mukesh Yadav
Shaza Tizani
Basant Bhandari
Anthony J Valente
The University of Texas Health Science Center at San Antonio · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Exposure of proximal tubular epithelial cells to high glucose contributes to the accumulation of tubulointerstitial and matrix proteins in diabetic nephropathy, but how this occurs is not well understood. We investigated the effect of the signaling molecule tuberin, which modulates the mammalian target of rapamycin pathway, on renal hypertrophy and fibronectin expression. We found that the kidney mass was significantly greater in partially tuberin-deficient (TSC2(+/-) ) diabetic rats than wild-type diabetic rats. Furthermore, TSC2(+/-) rats exhibited significant increases in the basal levels of phospho-tuberin and fibronectin expression in the kidney cortex. Increased levels of phosphorylated tuberin associated with an increase in fibronectin expression in both wild-type and TSC2(+/-) diabetic rats. Treatment with insulin abrogated the diabetes-induced increase in fibronectin expression. In vitro, high glucose enhanced fibronectin expression in TSC2(+/-) primary proximal tubular epithelial cells; both inhibition of Akt and inhibition of the mammalian target of rapamycin could prevent this effect of glucose. In addition, forced expression of tuberin in tuberin-null cells abolished the expression of fibronectin protein. Taken together, these data suggest that tuberin plays a central role in the development of renal hypertrophy and in modulating the production of the matrix protein fibronectin in diabetes.

Indexed as

AnimalsBase SequenceCells, CulturedDiabetes Mellitus, Type 1Diabetic NephropathiesFibronectinsGene ExpressionGene TargetingGlucoseHypertrophyKidneyMaleModels, BiologicalPhosphorylationPromoter Regions, GeneticProto-Oncogene Proteins c-aktFibronectinsGlucosemTOR protein, ratProto-Oncogene Proteins c-aktRibosomal Protein S6 Kinases, 70-kDaRNA, MessengerSirolimusTOR Serine-Threonine KinasesTsc2 protein, ratTuberous Sclerosis Complex 2 ProteinTumor Suppressor Proteins

Identifiers

PMID22904348
PMCPMC3458468
OpenAlexW2135130510

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.