Evidence map›Paper›PMID 40837363›Full record

ArticleJournal of medical biochemistry2025

Unraveling genetic predisposition and oxidative stress in vitiligo development and the role of artificial intelligence (AI) in diagnosis and management.

Hristina Kocić, Torello Lotti, Tatjana Jevtović-Stoimenov, Uwe Wollina, Yan Valle, Stevo Lukić, Aleksandra Klisić

Abstract read
In one paragraph

Article in Journal of medical biochemistry, 2025. 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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0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

7 authors.

Hristina KocićUniversity Clinical Center Niš, Clinic for Dermatology, Niš.
Torello LottiUniversità degli Studi Guglielmo Marconi, Dipartimento di Scienze dela Comunicazione, Rome, Italy.
Tatjana Jevtović-StoimenovUniversity of Niš, Medical Faculty, Department of Biochemistry, Niš.
Uwe WollinaAcademic Teaching Hospital, Municipal Hospital Dresden, Department of Dermatology and Allergology, Dresden, Germany.
Yan ValleVitiligo Research Foundation, New York, USA.
Stevo LukićUniversity of Niš, Faculty of Medicine, Neurology Department, Niš.
Aleksandra KlisićUniversity of Montenegro, Faculty of Medicine, Podgorica, Montenegro.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vitiligo is an autoimmune disorder with a complex genetic and epigenetic aetiology, characterised by progressive skin depigmentation. Recent advancements in artificial intelligence (AI) have greatly impacted the understanding, diagnosis, and treatment of vitiligo. The genetic basis of vitiligo is linked to multiple single nucleotide polymorphisms (SNPs) in genes associated with immune function, apoptosis, and melanogenesis, necessitating the integration of AI for more efficient diagnostic tools and personalised therapies. Genome-wide association studies (GWAS) have identified approximately 50 vitiligo-susceptibility genes, including PTPN1, PTPN22, NLRP1, FASLG, and TYR. These genes influence the immune response and melanocyte function, with the transcription factor Nuclear Factor kappa B (NF-kB), playing a central role in inflammatory responses and redox signaling induced by oxidative stress, in conjunction with antioxidant enzymes such as GPx, GST, SOD, and CAT. AI technologies offer a promising avenue for diagnosing vitiligo by combining genetic, clinical, and imaging data, allowing for more accurate classification and personalised treatment strategies. By analysing vast datasets, AI algorithms can identify patterns within complex genetic markers and clinical features, facilitating earlier and more precise detection of vitiligo. Furthermore, AI-driven approaches can optimise therapeutic monitoring, enabling real-time treatment efficacy and disease progression assessment. Integrating AI in vitiligo genetic diagnostics can revolutionise the monitoring of the disorder, improving patient outcomes through personalised, data-driven interventions.

Indexed as

antioxidative enzymesartificial intelligence (AI)melaninoxidative stresssingle nucleotide polymorphisms (SNP)vitiligo

Identifiers

PMID40837363
PMCPMC12363352

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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.