Liu Tianqi, Xi Tianyu, Dong Xiaoqin, Xu Dong
The Second Clinical Medical College, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Department and Institute of Infectious Disease, Tongji Hospital, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Disease, Huazhong University of Science and Technology, Wuhan, China.
Biomol Biomed. 2025 Apr 26;25(6):1218-1232. doi: 10.17305/bb.2024.11085.
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.
慢性肝病（CLD）是一个重大的全球健康问题，会导致发病率和死亡率上升，并与皮肤色素沉着变化有关。面部色素沉着过多是CLD患者的常见特征，尽管这一现象背后的确切机制尚不清楚。黑色素由真黑素和褐黑素组成，在黑素细胞中合成。其生成受半胱氨酸水平影响，并由关键酶如酪氨酸酶（TYR）、酪氨酸酶相关蛋白1（TYRP1）和酪氨酸酶相关蛋白2（TYRP2）调节。黑素小体在黑素细胞内的运输主要依赖于F-肌动蛋白和微管的协同作用。然而，黑色素从黑素细胞转移到周围树突状细胞的机制仍需进一步研究。多种因素导致肝纤维化，包括氧化应激和炎性细胞因子。本文讨论了慢性肝病患者血清中升高的可能增加黑色素沉积的因素。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，并建议形成一个结合相关因素的评分系统以提高预测准确性。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并减少皮肤色素沉着，但其具体效果仍需进一步研究。未来的研究应集中于验证色素沉着变化与CLD进展之间联系的机制，并探索能够同时改善肝功能和皮肤色素沉着的治疗方法，最终目标是为患者带来更好的预后。
