Evidence map›Paper›PMID 28989700›Full record

ArticleToxicology research2017

Toxicological Implications of Mitochondrial Localization of CYP2E1.

Jessica H Hartman, Grover P Miller, Joel N Meyer

Open access · bronzeAbstract read
In one paragraph

Article in Toxicology research, 2017. 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
2.7field-weighted citation impact, top 12% 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, 31 citations in OpenAlex.

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  14. Effects of Real-Ambient PMFrontiers in pharmacology · 2021
    Article
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

3 authors at 2 institutions in 2 countries.

Jessica H HartmanNicholas School of the Environment, Duke University, Durham, NC.
Grover P MillerBiochemistry and Molecular Biology, University of Arkansas for Medical Sciences, Little Rock, AR.
Joel N MeyerNicholas School of the Environment, Duke University, Durham, NC.
Duke University · USUniversity of Arkansas for Medical Sciences · US

Funding

The Role of Mitochondrial DNA Damage in NeurodegenerationR01ES017540 · NIEHS · DUKE UNIVERSITY · PI MEYER, JOEL NEWMAN · 2011 to 2015
$1.8M
DATA AND TOOLS FOR MODELING METABOLISM AND REACTIVITYR01LM012222 · NLM · WASHINGTON UNIVERSITY · PI MILLER, GROVER P, SWAMIDASS, SANJAY JOSHUA · 2016 to 2019
$1.5M
Computationally modeling the impact of ontogeny on drug metabolic fateR01LM012482 · NLM · UNIV OF ARKANSAS FOR MED SCIS · PI MILLER, GROVER P, SWAMIDASS, SANJAY JOSHUA · 2016 to 2019
$1.3M
Role of Mitochondrial CYP2E1 in Chemical Exposure-Driven NeurodegenerationF32ES027306 · NIEHS · DUKE UNIVERSITY · PI HARTMAN, JESSICA HELENE · 2016 to 2018
$171k
NIEHS NIH HHS F32 ES027306NIEHS NIH HHS R01 ES017540NLM NIH HHS R01 LM012222NLM NIH HHS R01 LM012482
6 · The paper itself

Abstract

Cytochrome P450 2E1 (CYP2E1) metabolizes an extensive array of pollutants, drugs, and other small molecules, often resulting in bioactivation to reactive metabolites. Therefore, it is unsurprising that it has been the subject of decades of research publications and reviews. However, while CYP2E1 has historically been studied in the endoplasmic reticulum (erCYP2E1), active CYP2E1 is also present in mitochondria (mtCYP2E1). Relatively few studies have specifically focused on mtCYP2E1, but there is growing interest in this form of the enzyme as a driver in toxicological mechanisms given its activity and location. Many previous studies have linked total CYP2E1 to conditions that involve mitochondrial dysfunction (fasting, diabetes, non-alcoholic steatohepatitis, and obesity). Furthermore, a large number of reactive metabolites that are formed by CYP2E1 through metabolism of drugs and pollutants have been demonstrated to cause mitochondrial dysfunction. Finally, there appears to be significant inter-individual variability in targeting to the mitochondria, which could constitute a source of variability in individual response to exposures. This review discusses those outcomes, the biochemical properties and toxicological consequences of mtCYP2E1, and highlights important knowledge gaps and future directions. Overall, we feel that this exciting area of research is rich with new and important questions about the relationship between mtCYP2E1, mitochondrial dysfunction, and pathology.

Identifiers

PMID28989700
PMCPMC5627779
OpenAlexW2594988227

What OpenQuestion holds

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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.