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Медицинская библиотека · Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology · 2026

[Immunocyte energy metabolism imbalance and precision treatment in vitiligo: Mechanistic insights and advances in targeted intervention].

Hu Wen, Qiu Yun, Kang Xiaojing

СтатьяОбзорАннотация на английскомПеревод в очереди

Аннотация

Vitiligo is a common cutaneous depigmentation disorder with a complex pathogenesis involving multiple factors such as oxidative stress, immune response, and metabolic disorders. Recent studies have revealed that the impaired energy metabolism in immune cells is closely linked to the pathogenesis of vitiligo, with mitochondrial homeostasis disruption playing a central role. Mitochondria not only serve as the cellular energy hub but also critically regulate immune cell function and activity. Furthermore, T cells have been shown to play pivotal roles in the development of vitiligo. This review systematically summarizes the multidimensional regulatory mechanisms underlying mitochondrial dysfunction and immune cell metabolic imbalance in the onset and progression of vitiligo. It highlights recent advances in precision treatment and targeted interventions, evaluating the progress and limitations of current mitochondria-oriented strategies, including antioxidants, mitochondrial protectants, metabolic modulators, and genetic therapies. We further propose the concept of "mitochondrial phenotype-based stratification", emphasizing the future integration of multi-omics data and functional assessments to achieve layered precision therapy for vitiligo. This work aims to offer novel insights and a theoretical foundation for the development of new treatment strategies and drug discovery in vitiligo.

Для цитирования: Hu Wen, Qiu Yun, Kang Xiaojing. [Immunocyte energy metabolism imbalance and precision treatment in vitiligo: Mechanistic insights and advances in targeted intervention].. Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology. 2026.

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