Evidence map›Paper›PMID 31894855›Full record

ArticleBioscience reports2020

Foam cells promote atherosclerosis progression by releasing CXCL12.

Lingxing Li, Zhenlan Du, Bing Rong, Dapeng Zhao, Aiping Wang, Yuzhen Xu, Huanyi Zhang, Xue Bai, Jingquan Zhong

Erratum issuedAbstract read
In one paragraph

Article in Bioscience reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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  15. Inflammatory Mediators in Atherosclerotic Vascular Remodeling.Frontiers in cardiovascular medicine · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors.

Lingxing Li *The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.
Zhenlan Du *Department of Cardiovascular Medicine, Tai'an City Central Hospital, Taian, China.
Bing RongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.
Dapeng ZhaoDepartment of Neurology, Tai'an City Central Hospital, Taian, China.
Aiping WangDepartment of Cardiovascular Medicine, Tai'an City Central Hospital, Taian, China.
Yuzhen XuDepartment of Neurology, Tai'an City Central Hospital, Taian, China.
Huanyi ZhangDepartment of Cardiovascular Medicine, Tai'an City Central Hospital, Taian, China.
Xue BaiDepartment of Cardiovascular Medicine, Tai'an City Central Hospital, Taian, China.
Jingquan ZhongThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Qilu Hospital of Shandong University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAtherosclerosis (AS) is a chronic inflammatory disease that contributes to multiple cardiovascular diseases (CVDs), and foam cell formation plays important roles in the progression of AS. There is an urgent need to identify new molecular targets for treating AS, and thereby improve the quality of life and reduce the financial burden of individuals with CVD.

methodsAn in vitro model of AS was generated by treating THP-1 cells and human aortic vascular smooth muscle cells (HA-VSMCs) with oxidized low-density lipoproteins (ox-LDLs). HA-VSMC proliferation and foam cell formation were detected by the MTT assay and Oil Red O staining. C-X-C motif chemokine 12 (CXCL12) expression was suppressed by siRNA. An AS rat model was established by feeding rats a high-fat diet and vitamin D2 for 3 weeks. Histopathology examinations were conducted by Hematoxylin and Eosin (H&E) staining and the levels ionized calcium-binding adapter molecule 1 (IBA1) and α smooth muscle actin (α-SMA) expression were determined by ELISA assays and immunohistochemistry.

resultsAn in vitro model of AS was established with THP-1 cells. CXCL12 expression in the model THP-1 cells was significantly increased when compared with its expression in control cells. Suppression of CXCL12 expression reduced the progression of AS in the cell model. Moreover, CXCL12 promoted AS in the in vivo rat model.

conclusionOur results suggest that CXCL12 plays an important role in promoting the progression of AS. Furthermore, inhibition of CXCL12 might suppress the development of AS by inhibiting HA-VSMC proliferation and their transformation to foam cells.

Indexed as

AnimalsAtherosclerosisCell ProliferationChemokine CXCL12Coculture TechniquesDiet, High-FatDisease Models, AnimalEndothelial CellsErgocalciferolsFoam CellsHumansLipoproteins, LDLMaleRats, Sprague-DawleySignal TransductionTHP-1 CellsChemokine CXCL12CXCL12 protein, humanCXCL12 protein, ratErgocalciferolsLipoproteins, LDLoxidized low density lipoproteinAtherosclerosisCXCL12foam cellmacrophage

Identifiers

PMID31894855
PMCPMC6970083

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Registered trials

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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 OpenQuestion graph.