Autophagy in psoriasis and vitiligo

Białczyk, Aleksandra; Czajkowski, Rafał

doi:10.5603/fd.a2022.0022

Cited by 2 publications

(3 citation statements)

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“…Furthermore, LC3 knockdown suppresses melanocyte-stimulating hormone (α-MSH)-mediated melanogenesis by reducing MITF expression and cAMP-response el-ement binding protein (CREB) phosphorylation [26]. In vitiligo, the loss of melanocytes might result from dysregulated autophagy-induced oxidative stress [28,29]. Adrenergic receptors and endothelin receptor type B (ETRB) employ protein kinase B (PKB) to increase tyrosinase (Tyr), tyrosinase-related protein 1 (TRP1) and tyrosinase-related protein 2 (TRP2) phosphorylation, leading to melanogenesis.…”

Section: Intrinsic Regulation Of Pigmentation In Melanocytesmentioning

confidence: 99%

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The Skin–Brain Axis: From UV and Pigmentation to Behaviour Modulation

Ascsillán,

Kemény

2024

IJMS

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The skin–brain axis has been suggested to play a role in several pathophysiological conditions, including opioid addiction, Parkinson’s disease and many others. Recent evidence suggests that pathways regulating skin pigmentation may directly and indirectly regulate behaviour. Conversely, CNS-driven neural and hormonal responses have been demonstrated to regulate pigmentation, e.g., under stress. Additionally, due to the shared neuroectodermal origins of the melanocytes and neurons in the CNS, certain CNS diseases may be linked to pigmentation-related changes due to common regulators, e.g., MC1R variations. Furthermore, the HPA analogue of the skin connects skin pigmentation to the endocrine system, thereby allowing the skin to index possible hormonal abnormalities visibly. In this review, insight is provided into skin pigment production and neuromelanin synthesis in the brain and recent findings are summarised on how signalling pathways in the skin, with a particular focus on pigmentation, are interconnected with the central nervous system. Thus, this review may supply a better understanding of the mechanism of several skin–brain associations in health and disease.

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Section: Intrinsic Regulation Of Pigmentation In Melanocytesmentioning

confidence: 99%

“…Furthermore, LC3 knockdown suppresses melanocyte-stimulating hormone (α-MSH)-mediated melanogenesis by reducing MITF expression and cAMP-response element binding protein (CREB) phosphorylation [ 26 ]. In vitiligo, the loss of melanocytes might result from dysregulated autophagy-induced oxidative stress [ 28 , 29 ].…”

Section: Pigmentation In Melanocytesmentioning

confidence: 99%

The Skin–Brain Axis: From UV and Pigmentation to Behaviour Modulation

Ascsillán,

Kemény

2024

IJMS

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“…It suggests that the KEAP1/Nrf2/ARE pathway may be one of the most important signalling pathways in protecting cells from oxidative stress. Furthermore, abnormalities in the Nrf2-p62 pathway also impair autophagy in vitiligo melanocytes under oxidative stress [ 28 , 29 ]. The role of Nrf2 gene polymorphisms in the susceptibility of patients to vitiligo and in altering the clinical presentation of the disease is also suspected [ 30 ].…”

Section: Oxidative Stressmentioning

confidence: 99%

Oxidative Stress and Potential Antioxidant Therapies in Vitiligo: A Narrative Review

Białczyk,

Wełniak,

Kamińska

et al. 2023

Mol Diagn Ther

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Vitiligo is a chronic skin disorder characterised by the loss of melanocytes and subsequent skin depigmentation. Although many theories have been proposed in the literature, none alone explains the pathogenesis of vitiligo. Oxidative stress has been identified as a potential factor in the pathogenesis of vitiligo. A growing body of evidence suggests that antioxidant therapies may offer a promising approach to managing this condition. This review summarises the potential mechanisms of oxidative stress and the types of melanocyte death in vitiligo. We also provide a brief overview of the most commonly studied antioxidants. Melanocytes in vitiligo are thought to be damaged by an accumulation of reactive oxygen species to destroy the structural and functional integrity of their DNA, lipids, and proteins. Various causes, including exogenous and endogenous stress factors, an imbalance between prooxidants and antioxidants, disruption of antioxidant pathways, and gene polymorphisms, lead to the overproduction of reactive oxygen species. Although necroptosis, pyroptosis, ferroptosis, and oxeiptosis are newer types of cell death that may contribute to the pathophysiology of vitiligo, apoptosis remains the most studied cell death mechanism in vitiligo. According to studies, vitamin E helps to treat lipid peroxidation of the skin caused by psoralen ultra-violet A treatment. In addition, Polypodium leucotomos increased the efficacy of psoralen ultra-violet A or narrow-band ultraviolet B therapy. Our review provides valuable insights into the potential role of oxidative stress in pathogenesis and antioxidant-based supporting therapies in treating vitiligo, offering a promising avenue for further research and the development of effective treatment strategies.

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Autophagy in psoriasis and vitiligo

Cited by 2 publications

References 0 publications

The Skin–Brain Axis: From UV and Pigmentation to Behaviour Modulation

The Skin–Brain Axis: From UV and Pigmentation to Behaviour Modulation

Oxidative Stress and Potential Antioxidant Therapies in Vitiligo: A Narrative Review

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