Research progress on pathogenesis of skin pigmentation in chronic liver disease.

0 MEDICINE, RESEARCH & EXPERIMENTAL Biomolecules & biomedicine Pub Date : 2025-04-26 DOI:10.17305/bb.2024.11085
Tianqi Liu, Tianyu Xi, Xiaoqin Dong, Dong Xu
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Abstract

Chronic liver disease (CLD) is a significant global health concern that leads to increased morbidity and mortality, and is associated with skin pigmentation changes. Excessive facial pigmentation is a common characteristic of patients with CLD, although the exact mechanism underlying this phenomenon remains unclear. Melanin, which consists of eumelanin and pheomelanin, is synthesized in melanocytes. Its production is influenced by cysteine levels and is regulated by key enzymes, such as tyrosinase (TYR), tyrosinase-related protein 1 (TYRP1), and tyrosinase-related protein 2 (TYRP2). The transport of melanosomes within melanocytes relies primarily on the coordinated action of F-actin and microtubules. However, the mechanism of melanin transfer from melanocytes to surrounding dendritic cells requires further investigation. Several factors contribute to liver fibrosis, including oxidative stress and inflammatory cytokines. This article discusses the factors that are elevated in the serum of patients with chronic liver disease, which may increase melanin deposition. It also introduces the signaling pathways related to melanin synthesis, providing indirect evidence for the pathological mechanisms underlying increased melanin synthesis in CLD. Additionally, the article points out that pigmentation may serve as an important indicator of liver disease deterioration and suggests the formation of a scoring system that combines related factors to enhance the predictive accuracy. In terms of treatment, antioxidants and anti-inflammatory drugs, such as silymarin and vitamin E, may improve CLD and reduce skin pigmentation, but their specific effects still require further investigation. Future research should focus on validating the mechanisms linking pigmentation changes with CLD progression, and exploring therapeutic methods that can simultaneously improve liver function and skin pigmentation, ultimately aiming for better patient outcomes.

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慢性肝病皮肤色素沉着的发病机制研究进展。
慢性肝病(CLD)是一个重大的全球健康问题,导致发病率和死亡率增加,并与皮肤色素沉着变化有关。过多的面部色素沉着是CLD患者的共同特征,尽管这种现象的确切机制尚不清楚。黑色素由真黑素和泛黑素组成,在黑色素细胞中合成。它的产生受半胱氨酸水平的影响,并受酪氨酸酶(TYR)、酪氨酸酶相关蛋白1 (TYRP1)和酪氨酸酶相关蛋白2 (TYRP2)等关键酶的调控。黑素小体在黑素细胞内的转运主要依赖于f -肌动蛋白和微管的协同作用。然而,黑色素从黑素细胞向周围树突状细胞转移的机制需要进一步研究。有几个因素导致肝纤维化,包括氧化应激和炎症细胞因子。本文探讨慢性肝病患者血清中增高的可能增加黑色素沉积的因子。它还介绍了与黑色素合成相关的信号通路,为CLD中黑色素合成增加的病理机制提供了间接证据。此外,文章指出色素沉着可能是肝病恶化的重要指标,并建议形成一个综合相关因素的评分系统,以提高预测的准确性。在治疗方面,抗氧化剂和抗炎药物,如水飞蓟素和维生素E,可能改善CLD和减少皮肤色素沉着,但其具体效果仍有待进一步研究。未来的研究应侧重于验证色素沉着变化与CLD进展之间的联系机制,并探索同时改善肝功能和皮肤色素沉着的治疗方法,最终以更好的患者预后为目标。
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