ArticleFrontiers in pediatrics2025
Genetic polymorphisms of antioxidant enzymes (GSTP1/CAT/HMOX1/EPHX1) and childhood asthma risk in Fuzhou.
Article in Frontiers in pediatrics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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.
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.
Who cites it
3 citing papers in PubMed.
- A Multilevel Redox-Based Prognostic Model for Asthma Severity: From Genotype to Serum Biomarkers.Biomedicines · 2026Review
- The Role of Oxidative Stress in the Pathogenesis of Childhood Asthma: A Comprehensive Review.Children (Basel, Switzerland) · 2025Review
- Decoding Asthma Therapy: The Role of VEGFA and HIF1A in Yanghe Pingchuan Granule's Mechanism.IET systems biologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Discuss the correlation between single nucleotide polymorphisms (SNPs) of the Glutathione s-transferase Pi-1 (GSTP1), Catalase (CAT), Heme oxygenase-1 (HMOX1), and Homo sapiens epoxide hydrolase 1 (EPHX1) genes and the risk of childhood asthma in Fuzhou. Methods: Next generation sequencing ( Results: The rs1695 A>G variant increased the risk of asthma in the heterozygous, dominant, and allele models. The rs4891 T>C variant increased the risk of asthma in the heterozygous, dominant, and allele models. The rs7943316 A>T variant increased the risk of asthma in the homozygous, recessive, and allele models. The rs769217 C>T variant decreased the risk of asthma in the homozygous, recessive, and allele models. Strong linkage disequilibrium between the GSTP1 gene rs1695 and rs4891, and the CAT gene rs7943316, rs1049982, and rs769217. The GC haplotype composed of GSTP1 gene rs1695 and rs4891 may pose a risk for childhood asthma [ Conclusion: The genotype GC, composed of GSTP1 gene rs1695 and rs4891, may represent a risk genotype for childhood asthma, whereas genotype AT may represent a protective genotype for childhood asthma. The genotype ATT, composed of CAT gene rs7943316, rs1049982, and rs769217, may represent a protective genotype for childhood asthma. The combination of GSTP1 gene rs1695 and CAT gene rs7943316 constitutes the optimal model for predicting the risk of childhood asthma in the Fuzhou region.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.