Evidence map›Paper›PMID 32194402›Full record

ReviewFrontiers in pharmacology2020

Chemokine Receptor 5, a Double-Edged Sword in Metabolic Syndrome and Cardiovascular Disease.

Zhongwen Zhang, Qiannan Wang, Jinming Yao, Xiaojun Zhou, Junyu Zhao, Xiaoqian Zhang, Jianjun Dong, Lin Liao

Abstract readReview
In one paragraph

Review in Frontiers in pharmacology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing 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

20 citing papers in PubMed.

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  13. Evidence from genetic studies among rs2107538 variant in theSaudi journal of biological sciences · 2023
    Article
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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.

Zhongwen ZhangDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Qiannan WangDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Jinming YaoDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Xiaojun ZhouDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Junyu ZhaoDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Xiaoqian ZhangDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.
Jianjun DongDivision of Endocrinology, Department of Internal Medicine, Qilu Hospital of Shandong University, Jinan, China.
Lin LiaoDepartment of Endocrinology, Shandong Provincial Qianfoshan Hospital, the First Hospital Affiliated with Shandong First Medical University, Jinan, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The key characteristic of cardiovascular disease (CVD) is endothelial dysfunction, which is likely the consequence of inflammation. It is well demonstrated that chemokines and their receptors play a crucial role in regulating inflammatory responses, and recently, much attention has been paid to chemokine receptor 5 (CCR5) and its ligands. For example, CCR5 aggravates the inflammatory response in adipose tissue by regulating macrophage recruitment and M1/M2 phenotype switch, thus causing insulin resistance and obesity. Inhibition of CCR5 expression reduces the aggregation of pro-atherogenic cytokines to the site of arterial injury. However, targeting CCR5 is not always effective, and emerging evidence has shown that CCR5 facilitates progenitor cell recruitment and promotes vascular endothelial cell repair. In this paper, we provide recent insights into the role of CCR5 and its ligands in metabolic syndrome as related to cardiovascular disease and the opportunities and roadblocks in targeting CCR5 and its ligands.

Indexed as

cardiovascular diseaseCCR5endothelial dysfunctioninflammationmetabolic syndrome

Identifiers

PMID32194402
PMCPMC7063056

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.