Evidence map›Paper›PMID 30973285›Full record

ArticleRenal failure2019

Label-free quantitative proteomics identifies Smarca4 is involved in vascular calcification.

Chan Wang, Yun Tang, Yanmei Wang, Guisen Li, Li Wang, Yi Li

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

Article in Renal failure, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 14% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 3 institutions in 1 country.

Chan Wanga Department of Nephrology , Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China , Chengdu , China.
Yun Tanga Department of Nephrology , Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China , Chengdu , China.
Yanmei Wangc Department of Nephrology , Affiliated Hospital of North Sichuan Medical College , Nanchong , China.
Guisen Lia Department of Nephrology , Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China , Chengdu , China.
Li Wanga Department of Nephrology , Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China , Chengdu , China.
Yi Lia Department of Nephrology , Sichuan Academy of Medical Sciences and Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China , Chengdu , China.
University of Electronic Science and Technology of China · CNSichuan Academy of Medical Sciences & Sichuan Provincial People's Hospital · CNAffiliated Hospital of North Sichuan Medical College · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular calcification (VC) is a pathological process characterized by abnormal deposition of calcium phosphate, hydroxyapatite and other mineral substances in the vascular wall. Hyperphosphorus is an important risk factor associated with VC in the general population and patients with chronic kidney disease (CKD). However, there is still a lack of early biomarkers for hyperphosphorus induced VC. We established a calcific rat aorta vascular smooth muscle cells (RASMCs) model by stimulating with β-glycerophosphate. Then we performed label-free quantitative proteomics combined with liquid chromatograph-mass spectrometer/mass spectrometer (LC-2D-MS/MS）analysis and bioinformatics analysis to find the potential biomarkers for VC. In the current study, we identified 113 significantly proteins. Fifty six of these proteins were significantly up-regulated and the other 57 proteins were significantly decreased in calcific RASMCs, compared to that of normal control cells (fold-change (fc)>1.2, p < .05). Bioinformatics analysis indicated that these significant proteins mainly involved in the placenta blood vessel development and liver regeneration. Their molecule function was cell adhesion molecule binding. Among them, Smarca4 is significantly up-regulated in calcific RASMCs with fc = 2.72 and p = .01. In addition, we also established VC rat model. Real-time quantitative PCR analysis confirmed that the expression of Smarca4 was significantly increased in the aorta of calcified rat. Consistent with the up-regulation of Smarca4, the expression of VC associated microRNA such as miR-133b and miR-155 was also increased. Consequently, our study demonstrates that Smarca4 is involved in hyperphosphorus-induced VC. This finding may contribute to the early diagnosis and prevention of VC.

Indexed as

AnimalsAortaBiomarkersCell LineDisease Models, AnimalDNA HelicasesGlycerophosphatesHumansHyperphosphatemiaKidney Failure, ChronicMaleMuscle, Smooth, VascularMyocytes, Smooth MuscleNuclear ProteinsPhosphatesProteomicsbeta-glycerophosphoric acidBiomarkersDNA HelicasesGlycerophosphatesNuclear ProteinsPhosphatesSmarca4 protein, ratTranscription Factorslabel-freeProteomicsSmarca4vascular calcification

Identifiers

PMID30973285
PMCPMC6461080
OpenAlexW2938030925

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.