Evidence map›Paper›PMID 33409276›Full record

ArticleFrontiers in cell and developmental biology2020

Reversal of Endothelial Extracellular Vesicle-Induced Smooth Muscle Phenotype Transition by Hypercholesterolemia Stimulation: Role of NLRP3 Inflammasome Activation.

Xinxu Yuan, Owais M Bhat, Arun Samidurai, Anindita Das, Yang Zhang, Pin-Lan Li

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cell and developmental biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.3field-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

19 citing papers in PubMed, 26 citations in OpenAlex.

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  12. Extracellular vesicles in vascular remodeling.Acta pharmacologica Sinica · 2022
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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

6 authors at 2 institutions in 1 country.

Xinxu YuanDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Owais M BhatDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Arun SamiduraiPauley Heart Center, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Anindita DasPauley Heart Center, Department of Internal Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Yang ZhangDepartment of Pharmacological and Pharmaceutical Sciences, College of Pharmacy, University of Houston, Houston, TX, United States.
Pin-Lan LiDepartment of Pharmacology and Toxicology, School of Medicine, Virginia Commonwealth University, Richmond, VA, United States.
Virginia Commonwealth University · USUniversity of Houston · US

Funding

Regulation of Lysosomes in Autophagy in Coronary Arterial MyocytesR01HL057244 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2001 to 2021
$6.7M
Subendothelial Exosomes in Coronary Microvascular DysfunctionR01HL075316 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2004 to 2024
$6.7M
Lysosome dysfunction in podocytopathy and associated hypertensionR01DK120491 · NIDDK · VIRGINIA COMMONWEALTH UNIVERSITY · PI LI, PINLAN · 2018 to 2022
$2.4M
Endothelial Inflammasomes in Coronary Microcirculation -Beyond InflammationR01HL122769 · NHLBI · VIRGINIA COMMONWEALTH UNIVERSITY · PI ZHANG, YANG · 2014 to 2018
$1.9M
MECHANISM OF CORONARY ENDOTHELIUM MEDIATED VASODILATIONR29HL057244 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI LI, PIN-LAN · 1997 to 2000
$101k
NHLBI NIH HHS R01 HL057244NHLBI NIH HHS R01 HL075316NHLBI NIH HHS R01 HL122769NHLBI NIH HHS R29 HL057244NIDDK NIH HHS R01 DK120491
6 · The paper itself

Abstract

Recent studies reported that vascular endothelial cells (ECs) secrete NLR family pyrin domain-containing 3 (NLRP3) inflammasome products such as interleukin-1β (IL-1β) via extracellular vesicles (EVs) under various pathological conditions. EVs represent one of the critical mechanisms mediating the cell-to-cell communication between ECs and vascular smooth muscle cells (VSMCs). However, whether or not the inflammasome-dependent EVs directly participate in the regulation of VSMC function remains unknown. In the present study, we found that in cultured carotid ECs, atherogenic stimulation by oxysterol 7-ketocholesterol (7-Ket) induced NLRP3 inflammasome formation and activation, reduced lysosome-multivesicular bodies (MVBs) fusion, and increased secretion of EVs that contain inflammasome product IL-1β. These EC-derived IL-1β-containing EVs promoted synthetic phenotype transition of co-cultured VSMCs, whereas EVs from unstimulated ECs have the opposite effects. Moreover, acid ceramidase

Indexed as

acid ceramidaseceramideendothelial cellsextracellular vesicleslysosome

Identifiers

PMID33409276
PMCPMC7779768
OpenAlexW3116317669

What Socratic 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 Socratic graph.