Evidence map›Paper›PMID 28785068›Full record

ArticleScientific reports2017

Hypoxia induced mitogenic factor (HIMF) triggers angiogenesis by increasing interleukin-18 production in myoblasts.

Chen-Ming Su, I-Ching Wang, Shan-Chi Liu, Yi Sun, Lulu Jin, Shih-Wei Wang, Hsiang-Ping Lee, Wen-Pei Tseng, Chih-Hsin Tang

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.3field-weighted citation impact, top 17% 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, 16 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

9 authors at 6 institutions in 2 countries.

Chen-Ming SuDepartment of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China.
I-Ching WangGraduate Institute of Sports and Health, National Changhua University of Education, Changhua County, Taiwan.
Shan-Chi LiuGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan.
Yi SunDepartment of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China.
Lulu JinDepartment of Biomedical Sciences Laboratory, Affiliated Dongyang Hospital of Wenzhou Medical University, Dongyang, Zhejiang, China.
Shih-Wei WangDepartment of Medicine, Mackay Medical College, New Taipei City, Taiwan.
Hsiang-Ping LeeGraduate Institute of Chinese Medicine, China Medical University, Taichung, Taiwan.
Wen-Pei TsengGraduate Institute of Sports and Health, National Changhua University of Education, Changhua County, Taiwan. twp@cc.ncue.edu.tw.
Chih-Hsin TangGraduate Institute of Basic Medical Science, China Medical University, Taichung, Taiwan. chtang@mail.cmu.edu.tw.
China Medical University · TWDongyang People's Hospital · CNNational Changhua University of Education · TWChina Medical University Hospital · TWMackay Medical College · TWWenzhou Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammatory myopathy is a rare autoimmune muscle disorder. Treatment typically focuses on skeletal muscle weakness or inflammation within muscle, as well as complications of respiratory failure secondary to respiratory muscle weakness. Impaired respiratory muscle function contributes to increased dyspnea and reduced exercise capacity in pulmonary hypertension (PH), a debilitating condition that has few treatment options. The initiation and progression of PH is associated with inflammation and inflammatory cell recruitment and it is established that hypoxia-induced mitogenic factor (HIMF, also known as resistin-like molecule α), activates macrophages in PH. However, the relationship between HIMF and inflammatory myoblasts remains unclear. This study investigated the signaling pathway involved in interleukin-18 (IL-18) expression and its relationship with HIMF in cultured myoblasts. We found that HIMF increased IL-18 production in myoblasts and that secreted IL-18 promoted tube formation of the endothelial progenitor cells. We used the mouse xenograft model and the chick chorioallantoic membrane assay to further explore the role of HIMF in inflammatory myoblasts and angiogenesis in vivo. Thus, our study focused on the mechanism by which HIMF mediates IL-18 expression in myoblasts through angiogenesis in vitro and in vivo. Our findings provide an insight into HIMF functioning in inflammatory myoblasts.

Indexed as

Up-Regulation3-Phosphoinositide-Dependent Protein KinasesAnimalsCell LineDisease Models, AnimalEndothelial Progenitor CellsHumansIntercellular Signaling Peptides and ProteinsInterleukin-18MiceMyoblastsNeovascularization, PathologicProto-Oncogene Proteins c-aktSignal TransductionTranscription Factor AP-13-Phosphoinositide-Dependent Protein KinasesIntercellular Signaling Peptides and ProteinsInterleukin-18interleukin-18 binding proteinPdpk1 protein, mouseProto-Oncogene Proteins c-aktRetnla protein, mouseTranscription Factor AP-1

Identifiers

PMID28785068
PMCPMC5547156
OpenAlexW2740349381

What OpenQuestion holds

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LicenceCC BY
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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.