Evidence map›Paper›PMID 30377890›Full record

ArticleInflammation2019

ApoM-S1P Modulates Ox-LDL-Induced Inflammation Through the PI3K/Akt Signaling Pathway in HUVECs.

Zhi Zheng, Yongzhi Zeng, Xiao Zhu, Ying Tan, Yi Li, Qian Li, Guanghui Yi

Abstract read
PubMed Publisher
In one paragraph

Article in Inflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

29 citing papers in PubMed, 52 citations in OpenAlex.

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  16. Apolipoprotein M gene polymorphisms in childhood-onset type 1 diabetes in southern Brazil.International journal of biochemistry and molecular biology · 2023
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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

7 authors at 1 institution in 1 country.

Zhi ZhengInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Yongzhi ZengInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Xiao ZhuInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Ying TanInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Yi LiInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Qian LiInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China.
Guanghui YiInstitute of Cardiovascular Research, Key Laboratory for Atherosclerology of Hunan Province, University of South China, 28 W Changsheng Road, Hengyang, 421001, Hunan, China. ghyi6108@163.com.ORCID http://orcid.org/0000-0002-8050-5396
University of South China · CN

Funding

National Natural Science Foundation of China 81770490
6 · The paper itself

Abstract

Studies have shown that apolipoprotein M (apoM), the main carrier of sphingosine-1-phosphate (S1P), is closely related to lipid metabolism and inflammation. While there are many studies on apoM and lipid metabolism, little is known about the role of apoM in inflammation. Atherosclerosis is a chronic inflammatory process. To clarify what role apoM plays in atherosclerosis, we used oxidized low-density lipoprotein (ox-LDL) to induce an inflammatory model of atherosclerosis. Our preliminary results indicate that ox-LDL upregulates the expression of S1P receptor 2 (S1PR2) in human umbilical vein endothelial cells (HUVECs). Ox-LDL-induced HUVECs were treated with apoM-bound S1P (apoM-S1P), free S1P or apoM, and apoM-S1P was found to significantly inhibit the expression of inflammatory factors and adhesion molecules. In addition, apoM-S1P inhibits ox-LDL-induced cellular inflammation via S1PR2. Moreover, apoM-S1P induces phosphorylation of phosphatidylinositol 3-kinase (PI3K)/Akt, preventing nuclear translocation of nuclear factor-κB (NF-κB). PI3K-specific inhibitors and Akt inhibitors suppress apoM-S1P/S1PR2-induced interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) release and affect nuclear translocation of NF-κB. In conclusion, the results demonstrate for the first time that apoM-S1P inhibits ox-LDL-induced inflammation in HUVECs via the S1PR2-mediated PI3K/Akt signaling pathway. This finding may aid in the development of new treatments for atherosclerosis.

Indexed as

Apolipoproteins MAtherosclerosisCells, CulturedHumansHuman Umbilical Vein Endothelial CellsInflammationLipoproteins, LDLLysophospholipidsModels, BiologicalPhosphatidylinositol 3-KinaseProtein BindingProto-Oncogene Proteins c-aktReceptors, LysosphingolipidSignal TransductionSphingosineSphingosine-1-Phosphate ReceptorsApolipoproteins MLipoproteins, LDLLysophospholipidsoxidized low density lipoproteinPhosphatidylinositol 3-KinaseProto-Oncogene Proteins c-aktReceptors, LysosphingolipidS1PR2 protein, humanSphingosinesphingosine 1-phosphateSphingosine-1-Phosphate Receptorsadhesion moleculesapoM-S1Patherosclerosisinflammatory factorsox-LDL

Identifiers

PMID30377890
OpenAlexW2899005969

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.