Evidence map›Paper›PMID 25188917›Full record

ReviewCurrent opinion in lipidology2014

Endothelial dysfunction: the role of sterol regulatory element-binding protein-induced NOD-like receptor family pyrin domain-containing protein 3 inflammasome in atherosclerosis.

Zhen Chen, Marcy Martin, Zhao Li, John Y-J Shyy

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Current opinion in lipidology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

25 citing papers in PubMed, 37 citations in OpenAlex.

  1. Review
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  16. Article
  17. Novel Insights Into the NLRP 3 Inflammasome in Atherosclerosis.Journal of the American Heart Association · 2019
    Review
  18. Review
  19. Shear Stress Regulation of Endothelium: A Double-edged Sword.Journal of translational internal medicine · 2018
    Article
  20. Review
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 3 institutions in 2 countries.

Zhen ChenaDivision of Cardiology, Department of Medicine, University of California, San Diego, La Jolla, California bBiochemistry and Molecular Biology Graduate Program, University of California, Riverside, Riverside, California, USA cCardiovascular Research Center, Medical School, Xi'an Jiaotong University, Xi'an, People's Republic of China.
Marcy Martin
Zhao Li
John Y-J Shyy
University of California, Riverside · USUniversity of California San Diego · USXi'an Jiaotong University · CN

Funding

Systems Biology Analyses for Hemodynamic Regulation of Vascular HomeostasisR01HL108735 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHIEN, SHU, SHYY, JOHN YJ · 2012 to 2024
$13.4M
Shear Stress, AMPK, and Endothelial FunctionsR01HL089940 · NHLBI · UNIVERSITY OF CALIFORNIA RIVERSIDE · PI SHYY, JOHN YJ · 2009 to 2013
$1.9M
Shear stress, SIRT1, and Arterial StiffeningR01HL105318 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI SHYY, JOHN YJ · 2010 to 2013
$1.5M
Hypoxia-Suppressed Dicer and AGO1 Promote AngiogenesisK99HL122368 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI CHEN, ZHEN BOUMAN · 2014 to 2015
$268k
NHLBI NIH HHS HL105318NHLBI NIH HHS HL108735NHLBI NIH HHS HL89940NHLBI NIH HHS K99 HL122368NHLBI NIH HHS R01 HL089940NHLBI NIH HHS R01 HL105318NHLBI NIH HHS R01 HL108735
6 · The paper itself

Abstract

purpose of reviewGreat effort has been devoted to elucidate the molecular mechanisms by which inflammasome in macrophages contributes to atherosclerosis. Inflammasome in vascular endothelial cells and its causal relationship with endothelial dysfunction in atherosclerosis are less understood. Here, we review the recent studies of inflammasome and its activation in endothelial cells, and highlight such endothelial inflammatory response in atherosclerosis. RECENT

findingsInflammasomes are critical effectors in innate immunity, and their activation in macrophages and the arterial wall contributes to atherogenesis. Sterol regulatory element-binding protein 2, a master regulator in cholesterol biosynthesis, can be activated in a noncanonical manner, which leads to the activation of the NOD-like receptor family pyrin domain-containing protein inflammasome in macrophages and endothelial cells. Results from in-vitro and in-vivo models suggest that sterol regulatory element-binding protein 2 is a key molecule in aggravating proinflammatory responses in endothelial cells and promoting atherosclerosis. SUMMARY: The SREBP-induced NOD-like receptor family pyrin domain-containing protein inflammasome and its instigation of innate immunity is an important contributor to atherosclerosis. Elucidating the underlying mechanisms will expand our understanding of endothelial dysfunction and its dynamic interaction with vascular inflammation. Furthermore, targeting SREBP-inflammasome pathways can be a therapeutic strategy for attenuating atherosclerosis.

Indexed as

AtherosclerosisCarrier ProteinsCholesterolEndothelial CellsGene Expression RegulationHumansImmunity, InnateMacrophagesNLR Family, Pyrin Domain-Containing 3 ProteinSterol Regulatory Element Binding Protein 2Carrier ProteinsCholesterolNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humanSterol Regulatory Element Binding Protein 2

Identifiers

PMID25188917
PMCPMC4339278
OpenAlexW2396184234

What OpenQuestion holds

Textmetadata
LicenceTDM
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.