Evidence map›Paper›PMID 32954825›Full record

ArticleAmerican journal of physiology. Endocrinology and metabolism2020

Long-chain acyl-CoA synthetase-1 mediates the palmitic acid-induced inflammatory response in human aortic endothelial cells.

Guang Ren, Sushant Bhatnagar, Daniel J Hahn, Jeong-A Kim

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Endocrinology and metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.6field-weighted citation impact, top 34% 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

10 citing papers in PubMed, 20 citations in OpenAlex.

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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.

Guang RenDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Alabama.
Sushant BhatnagarDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Alabama.
Daniel J HahnWilliams College, Williamstown, Massachusetts.
Jeong-A KimDepartment of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Alabama at Birmingham, Alabama.ORCID 0000-0003-4674-4606
University of Alabama at Birmingham · USWilliams College · US

Funding

University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
The role of Tomosyn-2 in insulin secretion and glucose toleranceR01DK120684 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Sushant Bhatnagar · 2019 to 2026
$2.6M
Saturated Fatty Acid-induced Autophagy in Vascular EndotheliumR01HL128695 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIM, JEONGA · 2016 to 2019
$1.8M
THE ROLE OF TOMOSYN-2 IN INSULIN SECRETIONR00DK095975 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI BHATNAGAR, SUSHANT · 2016 to 2018
$735k
Anti-obesity effect of NO-releasing NanomatrixR03AG058078 · NIA · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI KIM, JEONGA · 2018 to 2019
$149k
HHS | NIH | National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) R00 DK95975NHLBI NIH HHS R01 HL128695NIA NIH HHS R03 AG058078NIDDK NIH HHS P30 DK079626NIDDK NIH HHS R00 DK095975NIDDK NIH HHS R01 DK120684
6 · The paper itself

Abstract

Saturated fatty acid (SFA) induces proinflammatory response through a Toll-like receptor (TLR)-mediated mechanism, which is associated with cardiometabolic diseases such as obesity, insulin resistance, and endothelial dysfunction. Consistent with this notion, TLR2 or TLR4 knockout mice are protected from obesity-induced proinflammatory response and endothelial dysfunction. Although SFA causes endothelial dysfunction through TLR-mediated signaling pathways, the mechanisms underlying SFA-stimulated inflammatory response are not completely understood. To understand the proinflammatory response in vascular endothelial cells in high-lipid conditions, we compared the proinflammatory responses stimulated by palmitic acid (PA) and other canonical TLR agonists [lipopolysaccharide (LPS), Pam3-Cys-Ser-Lys4 (Pam

Indexed as

AortaCoenzyme A LigasesEndothelial CellsEndothelium, VascularE-SelectinHumansInflammationInsulinLipopolysaccharidesPalmitic AcidSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4TriazenesACSL1 protein, humanCoenzyme A LigasesE-SelectinInsulinLipopolysaccharidesPalmitic AcidTLR2 protein, humanToll-Like Receptor 2Toll-Like Receptor 4triacsin CTriazenesacyl-CoA synthetaseendothelial functioninflammationsaturated fatty acids

Identifiers

PMID32954825
PMCPMC7790120
OpenAlexW3087259147

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.