Evidence map›Paper›PMID 27188183›Full record

ArticleMolecular and cellular biochemistry2016

Globular CTRP9 inhibits oxLDL-induced inflammatory response in RAW 264.7 macrophages via AMPK activation.

Peng Zhang, Chengmin Huang, Jun Li, Tingting Li, Haipeng Guo, Tianjiao Liu, Na Li, Qing Zhu, Yuan Guo

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 46 citations in OpenAlex.

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  11. [Association between serum CTRP9 levels and diabetic retinopathy in patients with type 2 diabetes mellitus].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2021
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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 1 institution in 1 country.

Peng ZhangDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Chengmin HuangDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Jun LiDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Tingting LiDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Haipeng GuoThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Tianjiao LiuThe Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Qilu Hospital of Shandong University, Jinan, 250012, Shandong, China.
Na LiDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Qing ZhuDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China.
Yuan GuoDepartment of Cardiology, Qilu Hospital of Shandong University, 107 Wen Hua Xi Road, Jinan, 250012, Shandong Province, China. guoyuan9092@163.com.
Qilu Hospital of Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C1q-TNF-related protein-9 (CTRP9) is increasingly recognized as a promising cardioprotective adipocytokine, which regulates biological processes like vascular relaxation, proliferation, apoptosis, and inflammation. We recently showed that CTRP9 enhanced carotid plaque stability by reducing pro-inflammatory cytokines in macrophages. However, the underlying molecular mechanism of CTRP9 on anti-inflammatory response in macrophages still remains unclear. We demonstrated that globular CTRP9 (gCTRP9) significantly reduced oxidized low-density lipoprotein (oxLDL)-induced tumor necrosis factor alpha and monocyte chemoattractant protein 1 expression by suppressing nuclear factor-κB phosphorylation and nuclear translocation in RAW 264.7 macrophages. Treatment with gCTRP9 strikingly increased the level of phosphorylated adenosine monophosphate-activated protein kinase (AMPK). AMPK inhibitor abolished the anti-inflammatory effects of gCTRP9. Moreover, gCTRP9 increased the expression of adiponectin receptor 1 (AdipoR1). Downregulation of AdipoR1 by siRNA could abrogate the activation of AMPK and the anti-inflammatory effects of gCTRP9. These results suggested that gCTRP9 protected RAW 264.7 macrophages from oxLDL via AMPK activation in an AdipoR1 dependent fashion.

Indexed as

AdiponectinAMP-Activated Protein KinasesAnimalsCell LineEnzyme ActivationGlycoproteinsInflammationLipoproteins, LDLMacrophagesMiceReceptors, AdiponectinAdiponectinadiponectin receptor 1, mouseAMP-Activated Protein KinasesCTRP9 protein, mouseGlycoproteinsLipoproteins, LDLoxidized low density lipoproteinReceptors, AdiponectinAdipoR1AMPKCTRP9InflammationMacrophageNF-κB

Identifiers

PMID27188183
OpenAlexW2397457820

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.