Evidence mapPaperPMID 32016456Full record

ArticleMolecular medicine reports2020

The peptide compound urantide regulates collagen metabolism in atherosclerotic rat hearts and inhibits the JAK2/STAT3 pathway.

Tu Wang, Xiaoxu Sun, Haipeng Cui, Kai Liu, Juan Zhao

Open access · hybridAbstract read
In one paragraph

Article in Molecular medicine reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

3 citing papers in PubMed, 9 citations in OpenAlex.

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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.

Tu Wang *Department of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Xiaoxu Sun *Department of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Haipeng CuiDepartment of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Kai LiuDepartment of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Juan ZhaoDepartment of Pathophysiology, Chengde Medical University, Chengde, Hebei 067000, P.R. China.
Chengde Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the effect of urantide on collagen metabolism in the hearts of rats with atherosclerosis (AS) by evaluating the expression of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway constituents. Urantide was delivered to rats with AS via tail vein injection for 3, 7 and 14 days. Serological indicators were identified by an automated biochemical analyzer. Histomorphological changes in the cardiac tissue of rats were observed by pathological staining techniques. The expression of genes and proteins was assessed using reverse transcription‑quantitative PCR and western blot analysis, respectively. Localization of proteins was detected by immunofluorescence. Overexpression of urotensin II (UII) and its receptor, G protein‑coupled receptor 14 (GPR14), was observed in the hearts of rats with AS and the expression of both proteins significantly declined after urantide administration. Triglyceride, total cholesterol, low‑density lipoprotein, high‑density lipoprotein and calcium levels were improved in rats with AS following treatment with urantide. Notably, urantide was able to antagonize the UII/GPR14 system. Urantide treatment resulted in markedly decreased expression levels of matrix metalloproteinase 2 (MMP‑2), collagen type I/III, and genes and proteins in the JAK2/STAT3 pathway. By contrast, TIMP metallopeptidase inhibitor 2 (TIMP‑2) levels were increased. In addition, the MMP‑2/TIMP‑2 protein ratio was significantly decreased in rats treated with urantide compared with AS rats with no urantide treatment. Constituents of the JAK2/STAT3 pathway and collagen type I/III were found to be localized in the diseased tissue and blood vessels of the hearts of rats with AS. In conclusion, urantide was able to effectively block the UII/GPR14 system by regulating the JAK2/STAT3 pathway and collagen metabolism. Inhibition of the UII/GPR14 system may prevent and potentially treat atherosclerotic myocardial fibrosis. Based on the current results, it was hypothesized that collagen metabolism may be associated with the JAK2/STAT3 pathway.

Indexed as

AnimalsAorta, ThoracicAtherosclerosisCollagenDisease Models, AnimalFibrosisHeart DiseasesJanus Kinase 2Lipoproteins, LDLMaleMatrix Metalloproteinase 2Peptide FragmentsRatsReceptors, G-Protein-CoupledSignal TransductionSTAT3 Transcription FactorCollagenJak2 protein, ratJanus Kinase 2Lipoproteins, LDLMatrix Metalloproteinase 2Peptide FragmentsReceptors, G-Protein-CoupledStat3 protein, ratSTAT3 Transcription Factorurotensin IIurotensin II (4-11), Pen(5)-Trp(7)-Orn(8)-Urotensinsatherosclerosiscollagen metabolismJanus kinase 2/signal transducer and activator of transcription 3 pathwaymyocardial fibrosisurantideurotensin ii

Identifiers

PMID32016456
PMCPMC7003049
OpenAlexW2999847717

What Socratic holds

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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 Socratic graph.