Evidence map›Paper›PMID 29137283›Full record

ArticleOncotarget2017

C1q/Tumor necrosis factor-related protein-3 protects macrophages against LPS-induced lipid accumulation, inflammation and phenotype transition via PPARγ and TLR4-mediated pathways.

Jiale Lin, Qi Liu, Hui Zhang, Xingtao Huang, Ruoxi Zhang, Shuyuan Chen, Xuedong Wang, Bo Yu, Jingbo Hou

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2017. 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
2.2field-weighted citation impact, top 12% 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, 33 citations in OpenAlex.

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  11. CTRP3 Regulates Endochondral Ossification and Bone Remodeling During Fracture Healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2020
    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

9 authors at 2 institutions in 1 country.

Jiale LinDepartment 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, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xingtao HuangDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Ruoxi ZhangDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Shuyuan ChenDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Xuedong WangDepartment 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.
Jingbo HouDepartment of Cardiology, The Second Affiliated Hospital of Harbin Medical University, Harbin, China.
Second Affiliated Hospital of Harbin Medical University · CNHarbin Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Macrophage inflammation and foam cell formation are critical events during the initiation and development of atherosclerosis (AS). C1q/tumor necrosis factor-related protein-3 (CTRP3) is a novel adipokine with anti-inflammatory and cardioprotection properties; however, little is known regarding the influence of CTRP3 on AS. As macrophages play a key role in AS, this study investigated the effects of CTRP3 on macrophage lipid metabolism, inflammatory reactions, and phenotype transition, as well as underlying mechanisms, to reveal the relationship between CTRP3 and AS. CTRP3 reduced the number of lipid droplets, lowered cholesteryl ester (CE), total cholesterol (TC), and free cholesterol (FC) levels, reduced the CE/TC ratio, and dose-dependently inhibited TNFα, IL-6, MCP-1, MMP-9 and IL-1β release in lipopolysaccharide (LPS)-stimulated THP-1 macrophages and mouse peritoneal macrophages. Pretreatment with CTRP3 effectively increased macrophage transformation to M2 macrophages rather than M1 macrophages. Western blotting showed that the specific NF-κB pathway inhibitor ammonium pyrrolidine dithiocarbamate (PDTC) or siRNA targeting PPARγ/LXRα markedly strengthened or abolished the above-mentioned effects of CTRP3, respectively. These results show that CTRP3 inhibits TLR4-NF-κB pro-inflammatory pathways but activates the PPARγ-LXRα-ABCA1/ABCG1 cholesterol efflux pathway. Taken together, CTRP3 participates in anti-lipid accumulation, anti-inflammation and macrophage phenotype conversion via the TLR4-NF-κB and PPARγ-LXRα-ABCA1/ABCG1 pathways and, thus, may have anti-atherosclerotic properties.

Indexed as

atherosclerosisC1q/tumor necrosis factor-related protein-3 (CTRP3)cholesterol effluxinflammationmacrophage phenotype

Identifiers

PMID29137283
PMCPMC5669909
OpenAlexW2740383563

What OpenQuestion holds

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LicenceCC BY
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.