Evidence map›Paper›PMID 19590965›Full record

ReviewThe AAPS journal2009

Insights into the substrate specificity, inhibitors, regulation, and polymorphisms and the clinical impact of human cytochrome P450 1A2.

Shu-Feng Zhou, Li-Ping Yang, Zhi-Wei Zhou, Ya-He Liu, Eli Chan

Open access · bronzeAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in The AAPS journal, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed, 2 pooled it
13.8field-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

74 citing papers in PubMed, 2 syntheses or guidelines pooled it, 234 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. DDIapp-A Web-Based Application for Static Drug-Drug Interaction Assessment.CPT: pharmacometrics & systems pharmacology · 2026
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  14. Toxic effects ofFrontiers in toxicology · 2025
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14 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

5 authors at 3 institutions in 3 countries.

Shu-Feng ZhouDiscipline of Chinese Medicine, School of Health Sciences, WHO Collaborating Center for Traditional Medicine, RMIT University, Bundoora, Victoria, Australia. shufeng.zhou@rmit.edu.au
Li-Ping Yang
Zhi-Wei Zhou
Ya-He Liu
Eli Chan
RMIT University · AUBeijing Hospital · CNNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human CYP1A2 is one of the major CYPs in human liver and metabolizes a variety of clinically important drugs (e.g., clozapine, tacrine, tizanidine, and theophylline), a number of procarcinogens (e.g. benzo[a]pyrene and aflatoxin B(1)), and several important endogenous compounds (e.g. steroids and arachidonic acids). Like many of other CYPs, CYP1A2 is subject to induction and inhibition by a number of compounds, which may provide an explanation for some drug interactions observed in clinical practice. A large interindividual variability in the expression and activity of CYP1A2 and elimination of drugs that are mainly metabolized by CYP1A2 has been observed, which is largely caused by genetic (e.g., SNPs) and epigenetic (e.g., DNA methylation) and environmental factors (e.g., smoking and comedication). CYP1A2 is primarily regulated by the aromatic hydrocarbon receptor (AhR) and CYP1A2 is induced through AhR-mediated transactivation following ligand binding and nuclear translocation. To date, more than 15 variant alleles and a series of subvariants of the CYP1A2 gene have been identified and some of they have been associated with altered drug clearance and response to drug therapy. For example, lack of response to clozapine therapy due to low plasma drug levels has been reported in smokers harboring the -163A/A genotype; there is an association between CYP1A2*1F (-163C>A) allele and the risk for leflunomide-induced host toxicity. The *1F allele is associated with increased enzyme inducibility whereas *1C causes reduced inducibility. Further studies are warranted to explore the clinical and toxicological significance of altered CYP1A2 expression and activity caused by genetic, epigenetic, and environmental factors.

Indexed as

Gene Expression Regulation, EnzymologicPolymorphism, Single NucleotideSignal TransductionAnimalsCytochrome P-450 CYP1A2Cytochrome P-450 CYP1A2 InhibitorsEnzyme InhibitorsHumansMiceMice, KnockoutModels, MolecularSubstrate SpecificityCytochrome P-450 CYP1A2Cytochrome P-450 CYP1A2 InhibitorsEnzyme Inhibitors

Identifiers

PMID19590965
PMCPMC2758120
OpenAlexW2115459289

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.