Evidence map›Paper›PMID 28587104›Full record

ArticleInternational journal of molecular sciences2017

C1q/TNF-Related Protein-9 Ameliorates Ox-LDL-Induced Endothelial Dysfunction via PGC-1α/AMPK-Mediated Antioxidant Enzyme Induction.

Haijian Sun, Xuexue Zhu, Yuetao Zhou, Weiwei Cai, Liying Qiu

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.8field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Article
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  15. Adipokines, adiposity, and atherosclerosis.Cellular and molecular life sciences : CMLS · 2022
    Review
  16. Article
  17. Review
  18. Article
  19. [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
    Article
  20. 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

5 authors at 1 institution in 1 country.

Haijian SunDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. haijsunjiangnan@jiangnan.edu.cn.
Xuexue ZhuDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. xxzjn@jiangnan.edu.cn.
Yuetao ZhouDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. yuetao.zhou@jiangnan.edu.cn.
Weiwei CaiDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. vivi_cha@jiangnan.edu.cn.
Liying QiuDepartment of Basic Medicine, Wuxi School of Medicine, Jiangnan University, Wuxi 214122, China. qiulydoc@jiangnan.edu.cn.
Jiangnan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oxidized low-density lipoprotein (ox-LDL) accumulation is one of the critical determinants in endothelial dysfunction in many cardiovascular diseases such as atherosclerosis. C1q/TNF-related protein 9 (CTRP9) is identified to be an adipocytokine with cardioprotective properties. However, the potential roles of CTRP9 in endothelial function remain largely elusive. In the present study, the effects of CTRP9 on the proliferation, apoptosis, migration, angiogenesis, nitric oxide (NO) production and oxidative stress in human umbilical vein endothelial cells (HUVECs) exposed to ox-LDL were investigated. We observed that treatment with ox-LDL inhibited the proliferation, migration, angiogenesis and the generation of NO, while stimulated the apoptosis and reactive oxygen species (ROS) production in HUVECs. Incubation of HUVECs with CTRP9 rescued ox-LDL-induced endothelial injury. CTRP9 treatment reversed ox-LDL-evoked decreases in antioxidant enzymes including heme oxygenase-1 (HO-1), nicotinamide adenine dinucleotide phosphate (NAD(P)H) dehydrogenase quinone 1, and glutamate-cysteine ligase (GCL), as well as endothelial nitric oxide synthase (eNOS). Furthermore, CTRP9 induced activation of peroxisome proliferator-activated receptor γ co-activator 1α (PGC1-α) and phosphorylation of adenosine monophosphate-activated protein kinase (AMPK). Of interest, AMPK inhibition or PGC1-α silencing abolished CTRP9-mediated antioxidant enzymes levels, eNOS expressions, and endothelial protective effects. Collectively, we provided the first evidence that CTRP9 attenuated ox-LDL-induced endothelial injury by antioxidant enzyme inductions dependent on PGC-1α/AMPK activation.

Indexed as

AdiponectinAMP-Activated Protein KinasesAntioxidantsApoptosisCell CycleCell MovementCell ProliferationEndotheliumGlycoproteinsHumansHuman Umbilical Vein Endothelial CellsLipoproteins, LDLNitric OxideNitric Oxide Synthase Type IIIOxidation-ReductionOxidative StressAdiponectinAMP-Activated Protein KinasesAntioxidantsC1QTNF9B protein, humanGlycoproteinsLipoproteins, LDLNitric OxideNitric Oxide Synthase Type IIIoxidized low density lipoproteinPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanReactive Oxygen SpeciesTumor Necrosis Factor Receptor-Associated Peptides and ProteinsAMPKCTRP9endothelial dysfunctionox-LDLPGC1-α

Identifiers

PMID28587104
PMCPMC5485929
OpenAlexW2616882223

What OpenQuestion holds

Textmetadata
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.