Evidence map›Paper›PMID 24224119›Full record

ArticleJournal of diabetes & metabolism2013

Thrombospondin-1 Deficiency Exacerbates the Pathogenesis of Diabetic Retinopathy.

Christine M Sorenson, Shoujian Wang, Robert Gendron, Hélène Paradis, Nader Sheibani

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of diabetes & metabolism, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

31 citing papers in PubMed, 44 citations in OpenAlex.

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  19. Retinal oxygen: from animals to humans.Progress in retinal and eye research · 2017
    Review
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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

5 authors at 1 institution in 1 country.

Christine M SorensonDepartment of Pediatrics, University of Wisconsin School of Medicine and Public Health, USA ; McPherson Eye Research Institute, University of Wisconsin School of Medicine and Public Health, USA.
Shoujian Wang
Robert Gendron
Hélène Paradis
Nader Sheibani
McPherson College · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
Integrated Multidisciplinary Strategies for Detection of Diabetic RetinopathiesRC4EY021357 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ASSADI, AMIR H, ASSADI-PORTER, FARIBA M · 2010 to 2010
$3.2M
PECAM-1 and Retinopathy of PrematurityR01EY016695 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI SHEIBANI, NADER · 2007 to 2011
$1.6M
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY016695NEI NIH HHS RC4 EY021357
6 · The paper itself

Abstract

Diabetic retinopathy is a leading cause of blindness in the United States. Access to new animal models that exhibit retinal vasculopathies with short duration of diabetes, are vital for understanding the underlying mechanisms and examining the efficacy of new treatment modalities. Our previous studies demonstrated decreased expression of Thrombospondin-1 (TSP1), an endogenous inhibitor of angiogenesis, in eyes from both patients and rodents with diabetes. Here we examined whether TSP1 deficiency could exacerbate diabetic retinal vasculopathies. Akita/+ male mice reproducibly develop diabetes by 4 weeks of age. These mice demonstrated the early non-proliferative stages of diabetic retinopathy, including decreased numbers of pericytes and increased glial cell activation. However, Akita/+ male mice deficient in TSP1 (Akita/+; TSP1-/-) demonstrated more advanced stages of diabetic retinopathy with a 4-fold increase in acellular capillaries and increased fibronectin and GFAP expression. These vascular changes were not attributable to aberrant retinal vascular development in the absence of TSP1, since down-regulation of TSP1 postnatally in the endothelium also resulted in more severe retinopathy. In addition, lack of another endogenous inhibitor of angiogenesis, pigment epithelium derived factor (PEDF), also enhanced diabetic retinopathy in Akita/+ mice. Akita/+; PEDF-/- male mice demonstrated increased numbers of acellular capillaries compared to controls but at a level lower than that observed in Akita/+; TSP1-/- mice. Thus, the exacerbation of diabetic retinopathy in Akita/+; TSP1-/- mice will allow the study of retinal vasculopathies with a shorter duration of diabetes and facilitate future testing of treatment modalities that protect the retinal vasculature and preserve sight.

Indexed as

Angiogenesis inhibitorsDiabetic retinopathyPEDFThrombospondin-1

Identifiers

PMID24224119
PMCPMC3818794
OpenAlexW161297482

What OpenQuestion holds

Textmetadata
LicenceTDM
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.