Evidence map›Paper›PMID 25762236›Full record

ReviewCurrent atherosclerosis reports2015

Sphingosine-1-phosphate receptor subtype 2 signaling in endothelial senescence-associated functional impairments and inflammation.

Jiawei Zhao, Dante Garcia, Allison Gartung, Menq-Jer Lee

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current atherosclerosis reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  4. Signal Transduction and Gene Regulation in the Endothelium.Cold Spring Harbor perspectives in medicine · 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

4 authors at 2 institutions in 1 country.

Jiawei ZhaoDepartment of Pathology, Cardiovascular Research Institute, Karmanos Cancer Institute, Wayne State University School of Medicine, 540 East Canfield Ave., Scott Hall 9215, Detroit, MI, 48201, USA, jzha@med.wayne.edu.
Dante Garcia
Allison Gartung
Menq-Jer Lee
Wayne State University · USThe Barbara Ann Karmanos Cancer Institute · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial inflammation is an important risk factor in the initiation and development of vascular disease. Therefore, signaling cascades and patho-physiological outcomes of endothelial inflammation are important questions in vascular biology. Recent studies suggest that sphingosine-1-phosphate receptor subtype 2 (S1PR2) signaling in endothelial cells (ECs) play a critical role in endothelial inflammation. For example, ECs present in atherosclerotic plaques exhibit senescence phenotype. Levels of S1PR2 are markedly increased in cultured senescent ECs and in lesion regions of atherosclerotic endothelium. Also, inflammatory cytokines and mechanical flow stress profoundly increase S1PR2 levels in ECs. Inhibition of endothelial S1PR2 signaling diminishes endothelial senescence-associated functional impairments and atherogenic stimuli-induced endothelial activation. In contrast, activation of endothelial S1PR2 stimulates the production of pro-inflammatory chemokines/cytokines and lipid mediators in ECs. In this article, we will review signaling and functions of sphingosine-1-phosphate (S1P) receptors in endothelial biology, with particular focus on endothelial S1PR2 signaling-mediated endothelial inflammation.

Indexed as

AnimalsAtherosclerosisCells, CulturedEndothelium, VascularHumansInflammationReceptors, LysosphingolipidSignal TransductionSphingosine-1-Phosphate ReceptorsReceptors, LysosphingolipidS1PR2 protein, humanSphingosine-1-Phosphate Receptors

Identifiers

PMID25762236
OpenAlexW2008969264

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.