Evidence map›Paper›PMID 29356931›Full record

ArticleInflammation2018

CX3CL1/CX3CR1 Axis Contributes to Angiotensin II-Induced Vascular Smooth Muscle Cell Proliferation and Inflammatory Cytokine Production.

Chengsheng Li, Jin He, Xiaoyi Zhong, Hua Gan, Yunfeng Xia

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.7field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 27 citations in OpenAlex.

  1. Article
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  11. Cytokine storm induced by SARS-CoV-2.Clinica chimica acta; international journal of clinical chemistry · 2020
    Review
  12. 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

5 authors at 2 institutions in 1 country.

Chengsheng LiDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Jin HeDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Xiaoyi ZhongDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Hua GanDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China.
Yunfeng XiaDepartment of Nephrology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, 400016, People's Republic of China. xyfcqmu@126.com.
First Affiliated Hospital of Chongqing Medical University · CNChongqing Medical University · CN

Funding

The Medical Research and Developmental Fund of the First Affiliated Hospital of Chongqing Medical University PYJJ2017-02Wu Jieping Medical Foundation 320.6750.16196
6 · The paper itself

Abstract

Angiotensin II (Ang II) dysregulation has been determined in many diseases. The CX3CL1/CX3CR1 axis, which has a key role in cardiovascular diseases, is involved in the proliferation and inflammatory cytokine production of vascular smooth muscle cells (VSMCs). In this study, we aim to explore whether Ang II has a role in the expression of CX3CL1/CX3CR1, thus contributing to the proliferation and pro-inflammatory status of VSMCs. Cultured mouse aortic VSMCs were stimulated with 100 nmol/L of Ang II, and the expression of CX3CR1 was assessed by western blot. The results demonstrated that Ang II significantly up-regulated CX3CR1 expression in VSMCs and induced the production of reactive oxygen species (ROS) and the phosphorylation of p38 MAPK. Inhibitors of NADPH oxidase, ROS, and AT1 receptor significantly reduced Ang II-induced CX3CR1 expression. Targeted disruption of CX3CR1 by transfection with siRNA significantly attenuated Ang II-induced VSMC proliferation as well as down-regulated the expression of proliferating cell nuclear antigen (PCNA). Furthermore, CX3CR1-siRNA suppressed the effect of Ang II on stimulating Akt phosphorylation. Besides, the use of CX3CR1-siRNA decreased inflammatory cytokine production induced by Ang II treatment. Our results indicate that Ang II up-regulates CX3CR1 expression in VSMCs via NADPH oxidase/ROS/p38 MAPK pathway and that CX3CL1/CX3CR1 axis contributes to the proliferative and pro-inflammatory effects of Ang II in VSMCs.

Indexed as

Angiotensin IIAnimalsCell ProliferationCells, CulturedChemokine CX3CL1CX3C Chemokine Receptor 1CytokinesInflammationMiceMuscle, Smooth, Vascularp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesAngiotensin IIChemokine CX3CL1CX3C Chemokine Receptor 1Cx3cl1 protein, mouseCx3cr1 protein, mouseCytokinesp38 Mitogen-Activated Protein KinasesReactive Oxygen SpeciesAngiotensin IICX3CR1InflammationProliferationVascular smooth muscle cells

Identifiers

PMID29356931
OpenAlexW2788433096

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.