Evidence map›Paper›PMID 22971995›Full record

ArticleKidney international2013

Tubular expression of heat-shock protein 27 inhibits fibrogenesis in obstructive nephropathy.

Aparna Vidyasagar, Shannon R Reese, Omeed Hafez, Ling-Jin Huang, William F Swain, Lynn M Jacobson, Jose R Torrealba, Pierre-Emmanuel Chammas, Nancy A Wilson, Arjang Djamali

Open access · greenAbstract read
In one paragraph

Article in Kidney international, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

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  12. Nox2 is a mediator of ischemia reperfusion injury.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2015
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Aparna VidyasagarDivision of Nephrology, University of Wisconsin School of Medicine and Public Health, Madison, WI 53705, USA.
Shannon R Reese
Omeed Hafez
Ling-Jin Huang
William F Swain
Lynn M Jacobson
Jose R Torrealba
Pierre-Emmanuel Chammas
Nancy A Wilson
Arjang Djamali
University of Wisconsin–Madison · US

Funding

The role of Nox2 in CNI-induced renal fibrosisR01DK092454 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI DJAMALI, ARJANG · 2011 to 2015
$1.7M
HSP27 in Kidney Epithelial to Mesenchymal TransformationK08DK067981 · NIDDK · UNIVERSITY OF WISCONSIN-MADISON · PI DJAMALI, ARJANG · 2004 to 2008
$587k
NIDDK NIH HHS K08 DK067981NIDDK NIH HHS R01 DK092454PHS HHS NIDDK-DK067981-5
6 · The paper itself

Abstract

Morphological changes that occur during kidney injury involve actin skeleton remodeling. Here we tested whether heat-shock protein 27 (HSP27), a small stress response protein involved in cytoskeletal remodeling, protects the kidney from tubulointerstitial fibrosis in obstructive nephropathy. Tubular cell HSP27 immunostaining was significantly increased in human kidneys with ureteropelvic junction obstruction, supporting the clinical relevance of our studies. To develop an animal model for mechanistic studies, we generated transgenic mice that specifically overexpress human HSP27 in renal tubules, under the kidney androgen-regulated protein promoter, and determined the effects of HSP27 overexpression on epithelial-to-mesenchymal transition and tubulointerstitial fibrosis following unilateral ureteral obstruction. This was associated with decreased fibrogenesis as evidenced by significant declines in phosphorylated p38MAPK, collagen III, α-smooth muscle actin, 4-hydroxynonenal, and reduced trichrome staining following obstruction. Notably, E-cadherin and β-catenin remained at the cell membrane of tubular cells in transgenic mice with an obstructed ureter. Monocyte/macrophage infiltration, however, was not significantly affected in these transgenic mice. Thus, tubular HSP27 inhibits fibrogenesis in obstructive nephropathy. Further studies are needed to determine pathways regulating the interactions between HSP27 and the E-cadherin-β-catenin complex.

Indexed as

Animalsbeta CateninCadherinsCell MembraneCollagen Type IIIDisease Models, AnimalEpithelial CellsEpithelial-Mesenchymal TransitionFemaleFibrosisHSP27 Heat-Shock ProteinsHumansKidney DiseasesKidney TubulesMaleMicebeta CateninCadherinsCollagen Type IIIHSP27 Heat-Shock Proteinsp38 Mitogen-Activated Protein Kinases

Identifiers

PMID22971995
PMCPMC3525804
OpenAlexW2033933546

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.