Evidence map›Paper›PMID 29979351›Full record

ArticleJournal of cardiovascular pharmacology2018

C1q/TNF-Related Protein 9 Inhibits THP-1 Macrophage Foam Cell Formation by Enhancing Autophagy.

Lu Zhang, Qi Liu, Hui Zhang, Xue-Dong Wang, Shu-Yuan Chen, Yang Yang, Hang Lv, Jing-Bo Hou, Bo Yu

Open access · hybridAbstract read
In one paragraph

Article in Journal of cardiovascular pharmacology, 2018. 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
2.6field-weighted citation impact, top 10% 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, 36 citations in OpenAlex.

  1. Article
  2. Review
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  5. Article
  6. Article
  7. Review
  8. Review
  9. Adipokines in atherosclerosis: unraveling complex roles.Frontiers in cardiovascular medicine · 2023
    Review
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
  16. Article
  17. Review
  18. Role of autophagy in atherosclerosis: foe or friend?Journal of inflammation (London, England) · 2019
    Review
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

9 authors at 1 institution in 1 country.

Lu ZhangDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Qi LiuDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Hui ZhangDepartment of Cardiology, Wenzhou Medical College-Affiliated Yiwu Central Hospital, Yiwu, China.
Xue-Dong WangDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shu-Yuan ChenDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Yang YangDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Hang LvDepartment of Cardiovascular Surgery, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Jing-Bo HouDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Bo YuDepartment of Cardiology, the Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Harbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the pathogenesis of early atherosclerosis, lipid-loaded macrophages are involved in plaque development and progression. As a novel adipokine, C1q/tumor necrosis factor-related protein-9 (CTRP9) has beneficial effects in cardiovascular disease. However, previous reports have not studied whether the formation of macrophage foam cell induced by oxidized low-density lipoprotein (ox-LDL) is affected by CTRP9. According to our study, in ox-LDL-induced THP-1 macrophages, CTRP9 could reduce the quantity of lipid droplets, lower the level of cholesteryl ester (CE), promote cholesterol efflux, as well as increase the expression level of the cholesterol transport receptors ATP-binding membrane cassette transporter A1 (ABCA1) and G1 (ABCG1). In addition, the protein of LC3 II is elevated and that of p62 is decreased in CTRP9-treated foam cells by enhancing autophagy. However, using 3-methyladenine (3-MA) abolished the role of CTRP9 by inhibiting autophagy. Mechanistically, the autophagy-promoting effects of CTRP9 on foam cells was reversed by an AMPK inhibitor, Compound C, which inhibited the signaling pathway of adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/mammalian target of rapamycin (mTOR). These results show that CTRP9 protects against atherosclerosis by promoting cholesterol efflux to reduce the formation of foam cell in virtue of inducing autophagy in an AMPK/mTOR signaling pathway-dependent manner.

Indexed as

AdiponectinAMP-Activated Protein KinasesATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1AutophagyCholesterolCholesterol EstersFoam CellsGlycoproteinsHumansLipid DropletsLipoproteins, LDLMicrotubule-Associated ProteinsRecombinant ProteinsSequestosome-1 ProteinSignal TransductionABCA1 protein, humanABCG1 protein, humanAdiponectinAMP-Activated Protein KinasesATP Binding Cassette Transporter 1ATP Binding Cassette Transporter, Subfamily G, Member 1C1QTNF9B protein, humanCholesterolCholesterol EstersGlycoproteinsLipoproteins, LDLMAP1LC3B protein, humanMicrotubule-Associated ProteinsMTOR protein, humanoxidized low density lipoproteinRecombinant ProteinsSequestosome-1 ProteinSQSTM1 protein, humanTOR Serine-Threonine KinasesTumor Necrosis Factor Receptor-Associated Peptides and Proteins

Identifiers

PMID29979351
PMCPMC6181274
OpenAlexW2809687632

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.