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Updated: Apr 21, 2026

Imaging Approaches to Assessments of Toxicological Oxidative Stress Using Genetically-encoded Fluorogenic Sensors
Published on: February 7, 2018
Causal effects of oxidative stress on hypertension: insights integrating multi-omics and colocalization analyses
Yue Zhang1, Jinyang Meng1, Yucheng Yan1
1School of Health Preservation and Rehabilitation, Chengdu University of Traditional Chinese Medicine, Chengdu, 611137, China.
Background And Aim:
Oxidative stress (OS) plays a role in hypertension development, but the underlying genetic mechanisms are not completely understood. This study aimed to investigate the association between OS-related genes and hypertension by performing an integrative multi-omics analysis using summary-data-based Mendelian randomization (SMR) and colocalization approaches.
Methods And Results:
We obtained OS-related genes, summary-level methylation and gene expression QTL data, GWAS statistics for hypertension from the GeneCards, European cohort studies, and FinnGen study, respectively. We used SMR, colocalization, GO and KEGG analyses to estimate the association between OS-related molecular signatures and hypertension. Our results showed that PRDX2, SLC25A13, CYP19A1, and SUMF1 were causally associated with risk of hypertension. Furthermore, we observed evidence of colocalization with hypertension for these genes in at least one omics layer. Higher expression of PRDX2 (hypomethylation of cg23467004/cg00155609), CYP19A1 (hypomethylation of cg14424631), and CYP2D6 (hypomethylation of cg04692870) was associated with a reduced risk of hypertension. Conversely, elevated expression of SLC25A13 (hypomethylation of cg21022364 and hypermethylation at cg18184880), PDGFB (hypermethylation of cg17961378/cg24990612), S100A9 (hypomethylation of cg15467116), CLN6 (hypomethylation of cg22576950/cg20716080 and hypermethylation of cg16038331/cg11750300), CLN8 (hypermethylation of cg23952859), GFPT1 (hypermethylation of cg25195673), ADH5 (hypermethylation of cg21548116), and SUMF1 (hypermethylation of cg24840601) increased the risk of hypertension. Enrichment analyses indicated that PI3K/Akt, MAPK, and Rap1 pathways play key roles in the OS mechanisms underlying hypertension.
Conclusions:
PRDX2, SLC25A13, SUMF1, and CYP19A1 may serve as potential therapeutic targets for hypertension. The PI3K/Akt, MAPK, and Rap1 pathways are important OS mechanisms in hypertension, and further validation is required.
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