Vitiligo DOI Creative Commons

Monisha Gupta

Pigment International, Journal Year: 2024, Volume and Issue: 11(3), P. 131 - 133

Published: Sept. 1, 2024

Metabolic anomalies in vitiligo: a new frontier for drug repurposing strategies DOI Creative Commons
Alessia Paganelli, Federica Papaccio, Mauro Picardo

et al.

Frontiers in Pharmacology, Journal Year: 2025, Volume and Issue: 16

Published: April 15, 2025

Vitiligo is a chronic autoimmune condition characterized by the destruction of melanocytes, leading to patchy loss skin depigmentation. Although its precise cause remains unclear, recent evidence suggests that metabolic disturbances, particularly oxidative stress and mitochondrial dysfunction, may play significant role in pathogenesis disease. Oxidative thought damage melanocytes trigger inflammatory responses, culminating melanocyte immune-mediate destruction. Additionally, patients with vitiligo often exhibit extra-cutaneous abnormalities such as abnormal glucose metabolism, dyslipidemia, high fasting plasma levels, blood pressure, out range C-peptide low biological antioxidant capacity, suggesting potential link between impairment development. This implies functional mirrors more general systemic targetable dysfunction. Notably, therapies targeting pathways, those involving peroxisome proliferator-activated nuclear receptor γ (PPARγ) agonists, are currently being investigated treatments for vitiligo. PPARγ activation restores membrane potential, DNA copy number and, consequently, ATP production. Moreover, agonists counteract stress, reduce inflammation, inhibit apoptosis, maintain fatty acid addition well-known capability enhance insulin sensitivity. increasing strong relationship alterations other approved anti-diabetic treatments, like metformin fibrates, treatment. Taken together, these data support use approaches alternative traditional immune-suppressive treatment

Language: Английский

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Vitiligo DOI Creative Commons

Monisha Gupta

Pigment International, Journal Year: 2024, Volume and Issue: 11(3), P. 131 - 133

Published: Sept. 1, 2024

Citations

0