Evidence map›Paper›PMID 26278389›Full record

ReviewCurrent molecular pharmacology2017

Alcoholic Liver Disease: from CYP2E1 to CYP2A5.

Tung Ming Leung, Yongke Lu

Abstract readReview
In one paragraph

Review in Current molecular pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.3field-weighted citation impact, top 22% 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

17 citing papers in PubMed, 37 citations in OpenAlex.

  1. Dietary Polyphenols fromNutrients · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Restoring energy metabolism by NADFood science & nutrition · 2024
    Article
  6. Article
  7. A Review: Cytochrome P450 in Alcoholic and Non-Alcoholic Fatty Liver Disease.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Review
  13. Article
  14. Review
  15. Article
  16. Chemical Components and Hepatoprotective Mechanism of Xwak Granule in Mice Treated with Acute Alcohol.Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
  17. Cytochrome P450s and Alcoholic Liver Disease.Current pharmaceutical design · 2018
    Review
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.

Tung Ming LeungGraduate Program in Public Health, Graduate School of Biomedical Sciences, Icahn School of Medicine at Mount. United States.
Yongke LuDepartment of Structural and Chemical Biology, Box 1677, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029. United States.
Icahn School of Medicine at Mount Sinai · US

Funding

CYP2A5 and alcoholic liver diseaseR21AA020877 · NIAAA · ICAHN SCHOOL OF MEDICINE AT MOUNT SINAI · PI LU, YONGKE · 2013 to 2014
$438k
NIAAA NIH HHS R21 AA020877
6 · The paper itself

Abstract

This article reviews recent studies on CYP2E1-mediated alcoholic liver injury, the induction of CYP2A5 by alcohol and the mechanism for this upregulation, especially the permissive role of CYP2E1 in the induction of CYP2A5 by alcohol and the CYP2E1-ROS-Nrf2 pathway, and protective effects of CYP2A5 against ethanol-induced oxidative liver injury. Ethanol can induce CYP2E1, an active generator of reactive oxygen species (ROS), and CYP2E1 is a contributing factor for alcoholinduced oxidative liver injury. CYP2A5, another isoform of cytochrome P450, can also be induced by ethanol. Chronic feeding of ethanol to wild type mice increased CYP2A5 catalytic activity, protein and mRNA levels as compared to pair-fed controls. This induction was blunted in CYP2E1 knockout (cyp2e1-/-) mice but was restored when human CYP2E1 was reintroduced and expressed in cyp2e1-/- mice. Ethanol-induced CYP2E1 co-localized with CYP2A5 and preceded the elevation of CYP2A5. The antioxidants N-acetyl cysteine and vitamin C lowered the alcohol elevation of ROS and blunted the alcohol induction of CYP2A5, but not CYP2E1, suggesting ROS play a novel role in the crosstalk between CYP2E1 and CYP2A5. The antioxidants blocked the activation of Nrf2, a transcription factor known to upregulate expression of CYP2A5. When alcohol-induced liver injury was enhanced in Nrf2 knockout (Nrf2-/-) mice, alcohol elevation of CYP2A5 but not CYP2E1 was also lower in Nrf2-/- mice. CYP2A5 knockout (cyp2a5-/-) mice exhibited an enhanced alcoholic liver injury compared with WT mice as indicated by serum ALT, steatosis and necroinflammation. Alcohol-induced hyperglycemia were observed in cyp2a5-/- mice but not in WT mice.

Indexed as

AnimalsAntioxidantsChemical and Drug Induced Liver InjuryCytochrome P-450 CYP2E1Cytochrome P450 Family 2HumansHyperglycemiaLiver Diseases, AlcoholicSignal TransductionUp-RegulationAntioxidantsCytochrome P-450 CYP2E1Cytochrome P450 Family 2AlcoholantioxidantsCYP2A5CYP2E1interactionsmouse liverNrf2reactive oxygen species

Identifiers

PMID26278389
PMCPMC5856453
OpenAlexW2210432373

What OpenQuestion holds

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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.