ArticleIrish journal of medical science2026
Apoptosis, inflammation, and oxidative/nitrosative stress-related miRNA expression in vitiligo patients.
Article in Irish journal of medical science, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundMelanocyte death in the pathogenesis of vitiligo is thought to be associated with ROS/RNS accumulation, but the interaction of miRNAs with oxidative and nitrosative stress is not yet clear.
aimThis study aimed to evaluate the role of miRNAs associated with oxidative stress, apoptosis, and melanogenesis in the pathogenesis of vitiligo and to determine the relationship between these miRNAs and plasma levels of oxidative/nitrosative stress biomarkers.
methodsThe study included 30 vitiligo patients and 30 healthy individuals. Expression levels of 34 specific miRNAs were measured by quantitative real-time PCR in plasma samples obtained from patients and controls. Catalase (CAT), superoxide dismutase (SOD), malondialdehyde (MDA), 3-nitrotyrosine (3-NT), and nitric oxide (NO) levels were measured to determine plasma and erythrocytic oxidative/nitrosative stress levels.
resultsWhile there was no significant difference in the levels of 5 miRNAs analyzed in vitiligo patients compared to the control group, expression levels of 29 miRNAs were up- or down-regulated, and the differences were statistically significant. Especially, changes in miR-34a-5p, miR-373-3p, miR-196a-5p, miR-25-3p, miR-26a-5p, miR-193a-5p, miR-146a-5p, and miR-223-3p were found to be statistically significant (p < 0.001). In addition, plasma MDA, NO, and 3-NT levels were significantly higher, and SOD and CAT enzyme activities were significantly lower in the vitiligo group.
conclusionsOur findings revealed significant changes in miRNA levels associated with melanocyte apoptosis, inflammation, oxidative stress, and melanogenesis, which play a role in the pathogenesis of vitiligo. Furthermore, increased oxidative and nitrosative stress responses support their role in the physiopathology of the disease.
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