Evidence map›Paper›PMID 29463607›Full record

ArticleJournal of lipid research2018

Reduced atherosclerosis lesion size, inflammatory response in miR-150 knockout mice via macrophage effects.

Fu-Han Gong, Wen-Lin Cheng, Haiping Wang, Maomao Gao, Juan-Juan Qin, Yan Zhang, Xia Li, Xueyong Zhu, Hao Xia, Zhi-Gang She

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

Article in Journal of lipid research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

22 citing papers in PubMed, 30 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

10 authors at 2 institutions in 1 country.

Fu-Han GongDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Wen-Lin ChengDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Haiping WangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Maomao GaoBasic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Juan-Juan QinBasic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Yan ZhangDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Xia LiBasic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Xueyong ZhuDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China.
Hao XiaDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China. Electronic address: xiahao1966@163.com.
Zhi-Gang SheDepartment of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, China; Basic Medical School and Medical Research Institute, School of Medicine, Wuhan University, Wuhan 430071, China; Institute of Model Animal of Wuhan University, Wuhan 430060, China. Electronic address: zgshe@whu.edu.cn.
Wuhan University · CNRenmin Hospital of Wuhan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis is considered to be a chronic inflammatory disease that can lead to severe clinically important cardiovascular events. miR-150 is a small noncoding RNA that significantly enhances inflammatory responses by upregulating endothelial cell proliferation and migration, as well as intravascular environmental homeostasis. However, the exact role of miR-150 in atherosclerosis remains unknown. Here, we investigated the effect of miR-150 deficiency on atherosclerosis development. Using double-knockout (miR-150

Indexed as

AnimalsAtherosclerosisInflammationLIM Domain ProteinsMacrophagesMaleMiceMice, Inbred C57BLMice, KnockoutMicroRNAsOxidation-ReductionTranscription FactorsUp-RegulationLdb2 protein, mouseLIM Domain ProteinsMicroRNAsMirn150 microRNA, mouseTranscription FactorsinflammationmicroRNA-150PDZ and LIM domain 1

Identifiers

PMID29463607
PMCPMC5880493
OpenAlexW2788482851

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.