Evidence map›Paper›PMID 34029211›Full record

ArticleAging2021

Curcumin inhibits the proliferation and migration of vascular smooth muscle cells by targeting the chemerin / CMKLR1 / LCN2 axis.

Yaqiong He, Rongning Wang, Peng Zhang, Jianlong Yan, Nan Gong, Yuhang Li, Shaohong Dong

Open access · hybridAbstract read
In one paragraph

Article in Aging, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

13 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  5. Review
  6. Review
  7. Article
  8. Chemerin is resident to vascular tunicas and contributes to vascular tone.American journal of physiology. Heart and circulatory physiology · 2023
    Article
  9. Review
  10. Article
  11. Review
  12. Review
  13. CMKLR-1 Expression in Human Aorta Is Dominated by Smooth Muscle Cell Positivity.The journal of histochemistry and cytochemistry : official journal of the Histochemistry Society
    Article
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

7 authors at 3 institutions in 1 country.

Yaqiong HeDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Rongning WangDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Peng ZhangDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Jianlong YanDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Nan GongDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Yuhang LiDepartment of Orthopedics, Third Affiliated Hospital of Sun Yat-Sen University, Guangzhou 510630, Guangdong, China.
Shaohong DongDepartment of Cardiology, Shenzhen People's Hospital, Jinan University, Shenzhen 518000, Guangdong, China.
Jinan University · CNShenZhen People’s Hospital · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis (AS) is a chronic progressive inflammatory disease and a leading cause of death worldwide. Being a novel adipokine, chemerin is reported to be positively correlated with the severity of AS, yet its underlying mechanisms in AS remains elusive. It is well-known that AS development is significantly attributed to abnormal proliferation and migration of vascular smooth muscle cells (VSMCs). Therefore, we investigated the role of the chemerin / chemokine-like receptor 1 (CMKLR1, chemerin receptor) signaling, and the potential therapeutic effect of curcumin in VSMCs proliferation and migration during AS by establishing a high fat diet (HFD) mouse model. We found that CMKLR1 was highly expressed in HFD-induced AS tissues and that its expression level was positively correlated with aortic proliferation. Knockdown of CMKLR1 significantly inhibited VSMCs proliferation and migration, as evidenced by the EdU-incorporation assay, wound healing assay, and the induction of proliferating cell nuclear antigen (PCNA) and matrix metalloproteinase-9 (MMP-9) expression. Furthermore, we discovered that Lipocalin-2 (LCN2) acts as a key factor involved in CMKLR1-mediated VSMCs proliferation and migration via the p38 / MAPK and Wnt / β-catenin signaling pathways, and we demonstrated that curcumin inhibits VSMCs proliferation and migration by inhibiting chemerin / CMKLR1 / LCN2, thereby reducing AS progression. Our findings suggest that chemerin / CMKLR1 activation promotes the development of AS; hence, targeting the chemerin / CMKLR1 / LCN2 signaling pathway may be a reasonable treatment modality for AS.

Indexed as

Signal TransductionAnimalsAortaApolipoproteins EAtherosclerosisCell MovementCell ProliferationChemokinesCurcuminDiet, High-FatGene Knockdown TechniquesIntercellular Signaling Peptides and ProteinsLipocalin-2MaleMiceMice, KnockoutApolipoproteins Echemerin protein, mouseChemokinesCMKLR1 protein, mouseCurcuminIntercellular Signaling Peptides and ProteinsLipocalin-2Receptors, ChemokineatherosclerosisCMKLR1curcuminLCN2VSMC

Identifiers

PMID34029211
PMCPMC8202847
OpenAlexW3164940535

What OpenQuestion holds

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LicenceCC BY
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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.