Evidence map›Paper›PMID 22474292›Full record

ArticleThe Journal of biological chemistry2012

Scleraxis modulates bone morphogenetic protein 4 (BMP4)-Smad1 protein-smooth muscle α-actin (SMA) signal transduction in diabetic nephropathy.

Hideharu Abe, Tatsuya Tominaga, Takeshi Matsubara, Naoko Abe, Seiji Kishi, Kojiro Nagai, Taichi Murakami, Toshikazu Araoka, Toshio Doi

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

19 citing papers in PubMed, 29 citations in OpenAlex.

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  6. The Role of Bone Morphogenetic Proteins in Diabetic Complications.ACS pharmacology & translational science · 2020
    Review
  7. Scleraxis lineage cells contribute to organized bridging tissue during tendon healing and identify a subpopulation of resident tendon cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
    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

9 authors at 2 institutions in 1 country.

Hideharu AbeDepartment of Nephrology, Institute of Health Biosciences, University of Tokushima Graduate School of Medicine, Tokushima 770-8503, Japan. abeabe@clin.med.tokushima-u.ac.jp
Tatsuya Tominaga
Takeshi Matsubara
Naoko Abe
Seiji Kishi
Kojiro Nagai
Taichi Murakami
Toshikazu Araoka
Toshio Doi
Tokushima University · JPKyoto University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Activation of mesangial cells (MCs), which is characterized by induction of smooth muscle α-actin (SMA) expression, contributes to a key event in various renal diseases; however, the mechanisms controlling MC differentiation are still largely undefined. Activated Smad1 induced SMA in a dose-dependent manner in MCs. As a direct regulating molecule for SMA, we identified and characterized scleraxis (Scx) as a new phenotype modulator in advanced glycation end product (AGE)-exposed MCs. Scx physically associated with E12 and bound the E-box in the promoter of SMA and negatively regulated the AGE-induced SMA expression. Scx induced expression and secretion of bone morphogenetic protein 4 (BMP4), thereby controlling the Smad1 activation in AGE-treated MCs. In diabetic mice, Scx was concomitantly expressed with SMA in the glomeruli. Inhibitor of differentiation 1 (Id1) was further induced by extended treatment with AGE, thereby dislodging Scx from the SMA promoter. These data suggest that Scx and Id1 are involved in the BMP4-Smad1-SMA signal transduction pathway besides the TGFβ1-Smad1-SMA signaling pathway and modulate phenotypic changes in MCs in diabetic nephropathy.

Indexed as

Signal TransductionActinsAnimalsBasic Helix-Loop-Helix ProteinsBone Morphogenetic Protein 4Diabetic NephropathiesGene Expression RegulationGlomerular MesangiumGlycation End Products, AdvancedInhibitor of Differentiation Protein 1MaleMiceResponse ElementsSmad1 ProteinTranscription Factor 3Transforming Growth Factor beta1ActinsBasic Helix-Loop-Helix ProteinsBmp4 protein, mouseBone Morphogenetic Protein 4Glycation End Products, AdvancedIdb1 protein, mouseInhibitor of Differentiation Protein 1Scx protein, mouseSmad1 ProteinSmad1 protein, mouseTranscription Factor 3Transforming Growth Factor beta1

Identifiers

PMID22474292
PMCPMC3370223
OpenAlexW1984495564

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.