Evidence map›Paper›PMID 31966509›Full record

ArticleInternational journal of clinical and experimental pathology2017

Adenovirus-expressing miR-153-3p alleviates aortic calcification in a rat model with chronic kidney disease.

Fenghua Yao, Li Zhang, Zhong Yin, Bo Fu, Zhe Feng, Zongze He, Qinggang Li, Jijun Li, Xiangmei Chen

Open access · greenAbstract read
In one paragraph

Article in International journal of clinical and experimental pathology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.2field-weighted citation impact, top 42% 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

2 citing papers in PubMed, 5 citations in OpenAlex.

  1. Review
  2. Article
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.

Fenghua YaoDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Li ZhangDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Zhong YinDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Bo FuDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Zhe FengDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Zongze HeDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Qinggang LiDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Jijun LiDepartment of Nephrology, First Hospital Affiliated to The Chinese PLA General Hospital Beijing, China.
Xiangmei ChenDepartment of Nephrology, Chinese PLA General Hospital, Chinese PLA Institute of Nephrology, State Key Laboratory of Kidney Diseases, National Clinical Research Center for Kidney Diseases Beijing, China.
Chinese PLA General Hospital · CNFirst Affiliated Hospital of Chinese PLA General Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundPatients with chronic kidney disease (CKD) have abnormal calcification in vascular tissue that is a risk factor for cardiovascular disease. However, the specific molecular mechanisms for vascular calcification remain largely unknown. The present study aimed to determine the differentially expressed miRs and the underlying molecular mechanisms of miR-153-3p in vascular calcification induced by adenine.

methodsDifferentially expressed miRs were screened using a microarray chip in the thoracic aorta. miRs and mRNA expression were measured by RT-qPCR. Protein expression was performed by western blotting analysis. Aortic calcification was confirmed by Von Kossa staining. The targeted genes were predicted by a bioinformatics algorithm and confirmed by a dual luciferase reporter assay.

resultsOur results revealed that the expression of miR-153-3p was significantly down-regulated in the thoracic aorta from adenine-fed rats compared with that of the control group. Transfection of miR-153-3p into the thoracic aorta markedly suppressed adenine-induced aortic calcification and significantly decreased the mRNA expression of ALP, OC, OSX, SOST and Runx2. Further studies indicated that Runx2 was a direct target gene of miR-153-3p, which was verified by dual luciferase reporter assay.

conclusionThese results suggest that increased vascular miR-153-3p expression attenuates adenine-induced aortic calcification via inhibiting osteogenic trans-differentiation in the thoracic aorta.

Indexed as

aortic calcificationmiR-153-3posteogenic trans-differentiationRunx2

Identifiers

PMID31966509
PMCPMC6966037
OpenAlexW3007764778

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.