Evidence map›Paper›PMID 23863467›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Thrombospondin 1 mediates renal dysfunction in a mouse model of high-fat diet-induced obesity.

Wenpeng Cui, Hasiyeti Maimaitiyiming, Xinyu Qi, Heather Norman, Shuxia Wang

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
3.0field-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

32 citing papers in PubMed, 46 citations in OpenAlex.

  1. Article
  2. Review
  3. Microbes and GFR in Health and CKD in Mice.Journal of the American Society of Nephrology : JASN · 2026
    Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Thrombospondin-1 CD47 Signalling: From Mechanisms to Medicine.International journal of molecular sciences · 2021
    Review
  9. Thrombospondin-1 in maladaptive aging responses: a concept whose time has come.American journal of physiology. Cell physiology · 2020
    Review
  10. Review
  11. Thrombospondin 1 and Its Diverse Roles as a Regulator of Extracellular Matrix in Fibrotic Disease.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society · 2019
    Review
  12. Article
  13. Article
  14. Article
  15. [Impacts of periodontitis on visceral organ weight and weight percentage in obese mice].Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology · 2018
    Article
  16. Thrombospondin-1 regulation of latent TGF-β activation: A therapeutic target for fibrotic disease.Matrix biology : journal of the International Society for Matrix Biology · 2018
    Review
  17. Review
  18. Review
  19. Role of thrombospondin 1 in liver diseases.Hepatology research : the official journal of the Japan Society of Hepatology · 2017
    Review
  20. Blockade of Orai1 Store-Operated Calcium Entry Protects against Renal Fibrosis.Journal of the American Society of Nephrology : JASN · 2016
    Article
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

5 authors at 2 institutions in 2 countries.

Wenpeng CuiGraduate Center for Nutritional Sciences, Univ. of Kentucky, Wethington Bldg. Rm. 583, 900 S. Limestone St., Lexington, KY 40536. swang7@uky.edu.
Hasiyeti Maimaitiyiming
Xinyu Qi
Heather Norman
Shuxia Wang
University of Kentucky · USJilin University · CN

Funding

THROMBOSPONDIN1 MEDIATES MACROPHAGE INFILTRATION INTO ADIPOSE TISSUE AND PROMOTEP20RR021954 · NCRR · UNIVERSITY OF KENTUCKY · PI ECKHARDT, ERIK · 2008 to 2011
$8.3M
TRAINING PROGRAM IN OXIDATIVE STRESS AND NUTRITIONT32DK007778 · NIDDK · UNIVERSITY OF KENTUCKY · PI WEBB, NANCY R · 2000 to 2019
$2.5M
Upstream Stimulatory Factor 2 regulation of renin in diabetic nephropathyR01DK081555 · NIDDK · UNIVERSITY OF KENTUCKY · PI WANG, SHUXIA · 2009 to 2013
$1.3M
NCRR NIH HHS P20RR021954NIDDK NIH HHS R01 DK 081555NIDDK NIH HHS R01 DK081555NIDDK NIH HHS T32 DK007778
6 · The paper itself

Abstract

Obesity is prevalent worldwide and is a major risk factor for many diseases including renal complications. Thrombospondin 1 (TSP1), a multifunctional extracellular matrix protein, plays an important role in diabetic kidney diseases. However, whether TSP1 plays a role in obesity-related kidney disease is unknown. In the present studies, the role of TSP1 in obesity-induced renal dysfunction was determined by using a diet-induced obese mouse model. The results demonstrated that TSP1 was significantly upregulated in the kidney from obese mice. The increased TSP1 was localized in the glomerular mesangium as well as in the tubular system from obese wild-type mice. Obese wild-type mice developed renal hypertrophy and albuminuria, which was associated with increased kidney macrophage infiltration, augmented kidney inflammation, and activated transforming growth factor (TGF)-β signaling and renal fibrosis. In contrast, obese TSP1-deficient mice did not develop these kidney damages. Furthermore, in vitro studies demonstrated that leptin treatment stimulated the expression of TSP1, TGF-β1, fibronectin, and collagen type IV in mesangial cells isolated from wild-type mice. These leptin-stimulated effects were abolished in TSP1-deficient mesangial cells. Taken together, these data suggest that TSP1 is an important mediator for obesity- or hyperleptinemia-induced kidney dysfunction.

Indexed as

AnimalsCells, CulturedCollagen Type IVDiabetic NephropathiesDiet, High-FatDisease Models, AnimalFibronectinsFibrosisKidneyLeptinMaleMiceNephritisObesityThrombospondin 1Transforming Growth Factor betaCollagen Type IVFibronectinsLeptinThbs1 protein, mouseThrombospondin 1Transforming Growth Factor betakidneyleptinobesitythrombospondin 1

Identifiers

PMID23863467
PMCPMC3761287
OpenAlexW2084388684

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.