Evidence map›Paper›PMID 30108504›Full record

ArticleFrontiers in pharmacology2018

Nrf2 Activation Provides Atheroprotection in Diabetic Mice Through Concerted Upregulation of Antioxidant, Anti-inflammatory, and Autophagy Mechanisms.

Iolanda Lazaro, Laura Lopez-Sanz, Susana Bernal, Ainhoa Oguiza, Carlota Recio, Ana Melgar, Luna Jimenez-Castilla, Jesus Egido, Julio Madrigal-Matute, Carmen Gomez-Guerrero

Open access · goldAbstract read
In one paragraph

Article in Frontiers in pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 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

10 authors at 3 institutions in 2 countries.

Iolanda LazaroRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Laura Lopez-SanzRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Susana BernalRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Ainhoa OguizaRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Carlota RecioRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Ana MelgarRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Luna Jimenez-CastillaRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Jesus EgidoRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Julio Madrigal-MatuteDepartment of Developmental and Molecular Biology, Institute for Aging Studies, Albert Einstein College of Medicine, New York City, NY, United States.
Carmen Gomez-GuerreroRenal, Vascular and Diabetes Research Lab, IIS-Fundacion Jimenez Diaz, Autonoma University of Madrid, Madrid, Spain.
Hospital Universitario Fundación Jiménez Díaz · ESUniversidad Autónoma de Madrid · ESAlbert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interactive relationships between metabolism, inflammation, oxidative stress, and autophagy in the vascular system play a key role in the pathogenesis of diabetic cardiovascular disease. Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a stress-sensitive guarantor of cellular homeostasis, which cytoprotective contributions extend beyond the antioxidant defense. We investigated the beneficial effects and underlying mechanisms of the Nrf2 inducer tert-butyl hydroquinone (tBHQ) on diabetes-driven atherosclerosis. In the experimental model of streptozotocin-induced diabetes in apolipoprotein E-deficient mice, treatment with tBHQ increased Nrf2 activity in macrophages and vascular smooth muscle cells within atherosclerotic lesions. Moreover, tBHQ significantly decreased the size, extension and lipid content of atheroma plaques, and attenuated inflammation by reducing lesional macrophages (total number and M1/M2 phenotype balance), foam cell size and chemokine expression. Atheroprotection was accompanied by both systemic and local antioxidant effects, characterized by lower levels of superoxide anion and oxidative DNA marker 8-hydroxy-2'-deoxyguanosine, reduced expression of NADPH oxidase subunits, and increased antioxidant capacity. Interestingly, tBHQ treatment upregulated the gene and protein expression of autophagy-related molecules and also enhanced autophagic flux in diabetic mouse aorta.

Indexed as

autophagydiabetes complicationsinflammationnuclear factor (erythroid-derived 2)-like 2redox balance

Identifiers

PMID30108504
PMCPMC6080546
OpenAlexW2886665056

What OpenQuestion holds

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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.