Update on the role of noncoding RNAs in vitiligo

Zhou, Ting; Dong, Li; Deng, Yansha

doi:10.1097/cm9.0000000000001900

Cited by 4 publications

(2 citation statements)

References 23 publications

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“…Additional potential players in mediating oxidative stress response are small non-coding RNAs (ncRNAs), especially microRNAs (miRNAs) [ 90 ]. miRNAs regulate post-transcriptional gene expression by inducing degradation or inhibiting translation of mRNA to proteins [ 91 ].…”

Section: Current Concepts In Immunopathogenesis Of Vitiligomentioning

confidence: 99%

Current Concepts of Vitiligo Immunopathogenesis

et al. 2022

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Vitiligo is an acquired immune-mediated disorder of pigmentation clinically characterized by well-defined depigmented or chalk-white macules and patches on the skin. The prevalence of vitiligo varies by geographical area, affecting 0.5% to 2% of the population. The disease imposes a significant psychological burden due to its major impact on patients’ social and emotional aspects of life. Given its autoimmune background, vitiligo is frequently associated with other autoimmune diseases or immune-mediated diseases. Vitiligo is a multifaceted disorder that involves both genetic predisposition and environmental triggers. In recent years, major predisposing genetic loci for the development of vitiligo have been discovered. The current findings emphasize the critical role of immune cells and their mediators in the immunopathogenesis of vitiligo. Oxidative-stress-mediated activation of innate immunity cells such as dendritic cells, natural killer, and ILC-1 cells is thought to be a key event in the early onset of vitiligo. Innate immunity cells serve as a bridge to adaptive immunity cells including T helper 1 cells, cytotoxic T cells and resident memory T cells. IFN-γ is the primary cytokine mediator that activates the JAK/STAT pathway, causing keratinocytes to produce the key chemokines CXCL9 and CXCL10. Complex interactions between immune and non-immune cells finally result in apoptosis of melanocytes. This paper summarizes current knowledge on the etiological and genetic factors that contribute to vitiligo, with a focus on immunopathogenesis and the key cellular and cytokine players in the disease’s inflammatory pathways.

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Section: Current Concepts In Immunopathogenesis Of Vitiligomentioning

confidence: 99%

Current Concepts of Vitiligo Immunopathogenesis

et al. 2022

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“…As this skin disorder manifests itself in altered and impaired appearance, the color differences manifested in exposed and sensitive areas often lead to high psychological stress, decreased quality of life and a strong desire for treatment [ 3 ]. The pathogenesis mainly includes genetic, autoimmune, mental and oxidative stress, endocrine dysfunction, and melanocyte shedding [ 4 , 5 , 6 , 7 ], but its exact pathogenesis is not yet clear, and its development is somewhat individualized and unpredictable. Vitiligo is one of the four major dermatological diseases that are easy to diagnose and difficult to treat [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

Optimization of Monobenzone-Induced Vitiligo Mouse Model by the Addition of Chronic Stress

Dong

Lai

Zhang

et al. 2023

IJMS

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Vitiligo is a common primary, limited or generalized skin depigmentation disorder. Its pathogenesis is complex, multifactorial and unclear. For this reason, few animal models can simulate the onset of vitiligo, and studies of drug interventions are limited. Studies have found that there may be a pathophysiological connection between mental factors and the development of vitiligo. At present, the construction methods of the vitiligo model mainly include chemical induction and autoimmune induction against melanocytes. Mental factors are not taken into account in existing models. Therefore, in this study, mental inducement was added to the monobenzone (MBEH)-induced vitiligo model. We determined that chronic unpredictable mild stress (CUMS) inhibited the melanogenesis of skin. MBEH inhibited melanin production without affecting the behavioral state of mice, but mice in the MBEH combined with CUMS (MC) group were depressed and demonstrated increased depigmentation of the skin. Further analysis of metabolic differences showed that all three models altered the metabolic profile of the skin. In summary, we successfully constructed a vitiligo mouse model induced by MBEH combined with CUMS, which may be better used in the evaluation and study of vitiligo drugs.

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