Evidence map›Paper›PMID 35959888›Full record

ArticleeLife2022

Inflammatory stress signaling via NF-

Joseph Wayne M Fowler, Rong Zhang, Bo Tao, Nabil E Boutagy, William C Sessa

Open access · goldAbstract read
In one paragraph

Article in eLife, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed, 1 pooled it
8.1field-weighted citation impact, top 2% 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

28 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  9. METTL16-mediated mJournal of experimental & clinical cancer research : CR · 2026
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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

5 authors at 1 institution in 1 country.

Joseph Wayne M FowlerVascular Biology and Therapeutics Program, Department of Pharmacology, Yale University School of Medicine, New Haven, United States.ORCID 0000-0001-5679-2236
Rong ZhangVascular Biology and Therapeutics Program, Department of Pharmacology, Yale University School of Medicine, New Haven, United States.
Bo TaoVascular Biology and Therapeutics Program, Department of Pharmacology, Yale University School of Medicine, New Haven, United States.
Nabil E BoutagyVascular Biology and Therapeutics Program, Department of Pharmacology, Yale University School of Medicine, New Haven, United States.
William C SessaVascular Biology and Therapeutics Program, Department of Pharmacology, Yale University School of Medicine, New Haven, United States.ORCID 0000-0001-5759-1938
Yale University · US

Funding

Surgery / Physiology CoreP01HL107205 · NHLBI · YALE UNIVERSITY · PI SIMONS, MICHAEL · 2012 to 2022
$18.8M
Insights into the Molecular and Cellular Mechanisms governing Endothelial FunctionR35HL139945 · NHLBI · YALE UNIVERSITY · PI SESSA, WILLIAM C · 2018 to 2021
$4.3M
Role of lipid droplets in insulin resistanceR01DK125492 · NIDDK · YALE UNIVERSITY · PI FERNANDEZ HERNANDO, CARLOS · 2020 to 2023
$1.8M
Endothelial lipid droplet turnover and regulation of metabolic functionK01DK124441 · NIDDK · YALE UNIVERSITY · PI BOUTAGY, NABIL · 2020 to 2022
$562k
NHLBI NIH HHS P01 HL107205NHLBI NIH HHS R35 HL139945NIDDK NIH HHS K01 DK124441NIDDK NIH HHS R01 DK125492
6 · The paper itself

Abstract

There is a growing appreciation that a tight relationship exists between cholesterol homeostasis and immunity in leukocytes; however, this relationship has not been deeply explored in the vascular endothelium. Endothelial cells (ECs) rapidly respond to extrinsic signals, such as tissue damage or microbial infection, by upregulating factors to activate and recruit circulating leukocytes to the site of injury and aberrant activation of ECs leads to inflammatory based diseases, such as multiple sclerosis and atherosclerosis. Here, we studied the role of cholesterol and a key transcription regulator of cholesterol homeostasis, SREBP2, in the EC responses to inflammatory stress. Treatment of primary human ECs with pro-inflammatory cytokines upregulated SREBP2 cleavage and cholesterol biosynthetic gene expression within the late phase of the acute inflammatory response. Furthermore, SREBP2 activation was dependent on NF-κB DNA binding and canonical SCAP-SREBP2 processing. Mechanistically, inflammatory activation of SREBP was mediated by a reduction in accessible cholesterol, leading to heightened sterol sensing and downstream SREBP2 cleavage. Detailed analysis of NF-κB inducible genes that may impact sterol sensing resulted in the identification of a novel

Indexed as

NF-kappa BCholesterolEndothelial CellsHumansInflammationSterol Regulatory Element Binding Protein 2SterolsStress, PhysiologicalTranscription, GeneticCholesterolNF-kappa BSREBF2 protein, humanSterol Regulatory Element Binding Protein 2SterolsALOD4cholesterolendothelialhumanimmunologyinflammationSREBP2

Identifiers

PMID35959888
PMCPMC9395194
OpenAlexW4293274153

What OpenQuestion 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 OpenQuestion graph.