Evidence map›Paper›PMID 24024137›Full record

ArticleRedox biology2013

Oxidized lipids activate autophagy in a JNK-dependent manner by stimulating the endoplasmic reticulum stress response.

Petra Haberzettl, Bradford G Hill

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 104 papers.

0numbers the graph read from it
0cells of the map it votes in
104citing papers in PubMed
12.2field-weighted citation impact, top 1% 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

104 citing papers in PubMed, 185 citations in OpenAlex.

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44 more citing papers are in PubMed but not listed here.

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

2 authors at 1 institution in 1 country.

Petra HaberzettlDiabetes and Obesity Center, Institute of Molecular Cardiology, University of Louisville, Louisville, KY, USA.
Bradford G Hill
University of Louisville · US

Funding

STEM CELLS AND DIABETIC CARDIOMYOPATHY PROJ 2 2009P20RR024489 · NCRR · UNIVERSITY OF LOUISVILLE · PI BHATNAGAR, ARUNI · 2008 to 2011
$10.0M
NCRR NIH HHS P20 RR024489NCRR NIH HHS RR24489
6 · The paper itself

Abstract

Excessive production of unsaturated aldehydes from oxidized lipoproteins and membrane lipids is a characteristic feature of cardiovascular disease. Our previous studies show that unsaturated lipid peroxidation-derived aldehydes such as 4-hydroxy-trans-2-nonenal (HNE) promote autophagy in rat aortic smooth muscle cells (RASMC). In this study, we examined the mechanism by which HNE induces autophagy. Exposure of RASMC to HNE led to the modification of several proteins, most of which were identified by mass spectrometry and confocal microscopy to be localized to the endoplasmic reticulum (ER). HNE stimulated the phosphorylation of PKR-like ER kinase and eukaryotic initiation factor 2α and increased heme oxygenase-1 (HO-1) abundance. HNE treatment also increased LC3-II formation and the phosphorylation of JNK and p38. Pharmacological inhibition of JNK, but not p38, prevented HNE-induced HO-1 expression and LC3-II formation. Inhibition of JNK increased cell death in HNE-treated cells. Pretreatment with the chemical chaperone phenylbutryic acid prevented LC3-II formation as well as JNK phosphorylation and HO-1 induction. Taken together, these data suggest that autophagic responses triggered by unsaturated aldehydes could be attributed, in part, to ER stress, which stimulates autophagy by a JNK-dependent mechanism and promotes cell survival during oxidative stress.

Indexed as

AutophagyAldehydesAnimalsAnthracenesAortaCells, CulturedEndoplasmic Reticulum StressGene Expression RegulationLipid PeroxidationMAP Kinase Signaling SystemMitogen-Activated Protein Kinase 8Myocytes, Smooth MuscleRatsRats, Sprague-Dawley4-hydroxy-2-nonenalAldehydesAnthracenesMitogen-Activated Protein Kinase 8pyrazolanthrone4-hydroxynonenalATF6, activating transcription factor 6AutophagyDMEM, Delbucco's Eagle Modified MediumDMSO, dimethylsulfoxideDNPH, 2,4-dinitrophenylhydrazineDTT, dithiothreitolECL, enhanced chemiluminescenceeIF2α, elongation initiation factor 2 αER, endoplasmic reticulumFBS, fetal bovine serumGrp, glucose regulated proteinHEPES, 4-(2-hydroxyethyl)-1-piperazineethanesulfonic acidHNE, 4-hydroxy-trans-2-nonenalHRP, horseradish peroxidaseIRE, inositol requiring enzymeJNKJNK, c-jun N-terminal kinaseLC3, microtubule-associated protein 1 light chain 3NP-40, noniodet P40Oxidative stressPDI, protein disulfide isomerasePERK, PKR-like ER kinasePVDF, polyvinylidene fluorideRASMC, rat aortic smooth muscle cellsSDS, sodium dodecyl sulfateSmooth muscle cellsUnfolded protein responseUPR, unfolded protein response

Identifiers

PMID24024137
PMCPMC3757667
OpenAlexW2148563903

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.