Evidence map›Paper›PMID 25009774›Full record

ArticleRedox biology2014

Potential role of proteasome on c-jun related signaling in hypercholesterolemia induced atherosclerosis.

Erdi Sozen, Betul Karademir, Burak Yazgan, Perinur Bozaykut, Nesrin Kartal Ozer

Open access · goldAbstract read
In one paragraph

Article in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 citing papers in PubMed, 35 citations in OpenAlex.

  1. Monotropein resists atherosclerosis by reducing inflammation, oxidative stress, and abnormal proliferation and migration of vascular smooth muscle cells.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2025
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  12. Oxidative Stress: Harms and Benefits for Human Health.Oxidative medicine and cellular longevity · 2017
    Review
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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.

Erdi SozenDepartment of Biochemistry, Faculty of Medicine, Genetic and Metabolic Diseases Research Center (GEMHAM), Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Betul KarademirDepartment of Biochemistry, Faculty of Medicine, Genetic and Metabolic Diseases Research Center (GEMHAM), Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Burak YazganDepartment of Biochemistry, Faculty of Medicine, Genetic and Metabolic Diseases Research Center (GEMHAM), Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Perinur BozaykutDepartment of Biochemistry, Faculty of Medicine, Genetic and Metabolic Diseases Research Center (GEMHAM), Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Nesrin Kartal OzerDepartment of Biochemistry, Faculty of Medicine, Genetic and Metabolic Diseases Research Center (GEMHAM), Marmara University, 34668 Haydarpasa, Istanbul, Turkey.
Marmara University · TR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Atherosclerosis and its complications are major causes of death all over the world. One of the major risks of atherosclerosis is hypercholesterolemia. During atherosclerosis, oxidized low density lipoprotein (oxLDL) regulates CD36-mediated activation of c-jun amino terminal kinase-1 (JNK1) and modulates matrix metalloproteinase (MMP) induction which stimulates inflammation with an invasion of monocytes. Additionally, inhibition of proteasome leads to an accumulation of c-jun and phosphorylated c-jun and activation of activator protein-1 (AP-1) related increase of MMP expression. We have previously reported a significant increase in cluster of differentiation 36 (CD36) mRNA levels in hypercholesterolemic rabbits and shown that vitamin E treatment prevented the cholesterol induced increase in CD36 mRNA expression. In the present study, our aim is to identify the signaling molecules/transcription factors involved in the progression of atherosclerosis following CD36 activation in an in vivo model of hypercholesterolemic (induced by 2% cholesterol containing diet) rabbits. In this direction, proteasomal activities by fluorometry and c-jun, phospo c-jun, JNK1, MMP-9 expressions by quantitative RT-PCR and immunoblotting were tested in aortic tissues. The effects of vitamin E on these changes were also investigated in this model. As a result, c-jun was phosphorylated following decreased proteasomal degradation in hypercholesterolemic group. MMP-9 expression was also increased in cholesterol group rabbits contributing to the development of atherosclerosis. In addition, vitamin E showed its effect by decreasing MMP-9 levels and phosphorylation of c-jun.

Indexed as

AnimalsAortaAtherosclerosisCholesterolCholesterol, DietaryGene ExpressionHypercholesterolemiaMaleMalondialdehydeMatrix Metalloproteinase 9Mitogen-Activated Protein Kinase 8PhosphorylationProteasome Endopeptidase ComplexRabbitsRNA, MessengerSignal TransductionCholesterolCholesterol, DietaryMalondialdehydeMatrix Metalloproteinase 9Mitogen-Activated Protein Kinase 8Proteasome Endopeptidase ComplexRNA, MessengerVitamin EAP-1AP-1, activator protein-1AtherosclerosisCD36, cluster of differentiation 36ERAD, endoplasmic-reticulum-associated protein degradationGAPDH, glyceraldehyde-3-phosphate dehydrogenaseHPLC, high-performance liquid chromatographyHypercholesterolemiaJNK1JNK, c-Jun amino terminal kinaseLDL, low density lipoproteinMAPK, mitogen-activated protein kinaseMDA, malondialdehydeMMP, matrix metallo proteinaseoxLDL, oxidized low density lipoproteinProteasomeTBA, thiobarbituric acidTNF a, tumor necrosis factor aUPS, ubiquitin-proteasome systemVitamin E

Identifiers

PMID25009774
PMCPMC4085352
OpenAlexW1968820512

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.