Evidence map›Paper›PMID 24690996›Full record

ArticleInternational journal of molecular sciences2014

BMP4 enhances foam cell formation by BMPR-2/Smad1/5/8 signaling.

Jun Feng, Jiangfei Gao, Yuxin Li, Yanhua Yang, Lili Dang, Yuanpeng Ye, Jingyuan Deng, Antai Li

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.1field-weighted citation impact, top 26% 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

18 citing papers in PubMed, 32 citations in OpenAlex.

  1. Endothelial BMP6 Drives Hemodynamic-Dependent VSMCs Calcification in Carotid Atherosclerosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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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

8 authors at 5 institutions in 1 country.

Jun FengDepartment of Cerebral Vessels, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China. junfengxian@163.com.
Jiangfei GaoDepartment of Neurology, Shangluo Central Hospital, Shangluo 726000, Shaanxi, China. jiangfei_gao@163.com.
Yuxin LiDepartment of Neurology, the Second Affiliated Hospital, Xi'an Medical College, Xi'an 710038, Shaanxi, China. yuxin_lisx@163.com.
Yanhua YangDepartment of Neurology, Shaanxi Armed Police Corps Hospital, Xi'an 710054, Shaanxi, China. yanhua_yangxa@163.com.
Lili DangDepartment of Neurology, Xingyuan Hospital, Yulin 719000, Shaanxi, China. lili_dang@163.com.
Yuanpeng YeDepartment of Cerebral Vessels, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China. yuanpeng_ye@163.com.
Jingyuan DengDepartment of Rehabilitation Medicine, First Affiliated Hospital of Medical College, Xi'an Jiaotong University, Xi'an 710061, Shaanxi, China. jingyuan_deng@163.com.
Antai LiDepartment of Neurology, Xi'an Central Hospital, Xi'an 710003, Shaanxi, China. antai_li@126.com.
First Affiliated Hospital of Xi'an Jiaotong University · CNShangluo Central Hospital · CNXian Central Hospital · CNXi'an Medical University · CNXiyuan Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis and its complications are characterized by lipid-laden foam cell formation. Recently, an obvious up-regulation of BMP4 was observed in atherosclerotic plaque, however, its function and the underlying mechanism remains unknown. In our study, BMP4 pretreatment induced macrophage foam cell formation. Furthermore, a dramatic increase in the ratio of cholesteryl ester (CE) to total cholesterol (TC) was observed in BMP4-treated macrophages, accompanied by the reduction of cholesterol outflow. Importantly, BMP4 stimulation inhibited the expression levels of the two most important cellular cholesterol transporters ABCA1 and ABCG1, indicating that BMP4 may induce formation of foam cells by attenuating transporters expression. Further mechanism analysis showed that BMPR-2, one of the BMP4 receptors, was significantly increased in BMP4 treated macrophage foam cells. That blocking its expression using specific siRNA significantly increased ABCA1 and ABCG1 levels. Additionally, BMP4 treatment triggered the activation of Smad1/5/8 pathway by BMPR-2 signaling. After blocking the Smad1/5/8 with its inhibitor, ABCA1 and ABCG1 expression levels were up-regulated significantly, suggesting that BMP4 inhibited the expression of ABCA1 and ABCG1 through the BMPR-2/Smad1/2/8 signaling pathway. Therefore, our results will provide a new insight about how BMP4 accelerate the progressio of atherosclerosis, and it may become a potential target against atherosclerosis and its complications.

Indexed as

AnimalsAtherosclerosisATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1Biological TransportBone Morphogenetic Protein 4Bone Morphogenetic Protein Receptors, Type IICell LineCholesterol EstersFoam CellsLipidsLipoproteinsMicePlaque, AtheroscleroticRNA InterferenceAbca1 protein, mouseABCG1 protein, mouseATP Binding Cassette Transporter 1ATP-Binding Cassette TransportersATP Binding Cassette Transporter, Subfamily G, Member 1Bmp4 protein, mouseBmpr2 protein, mouseBone Morphogenetic Protein 4Bone Morphogenetic Protein Receptors, Type IICholesterol EstersLipidsLipoproteinsRNA, Small InterferingSmad1 ProteinSmad1 protein, mouseSmad5 ProteinSmad5 protein, mouseSmad8 ProteinSmad9 protein, mouse

Identifiers

PMID24690996
PMCPMC4013580
OpenAlexW2067150453

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.