PDF(Pubmed)
Abstract：
Lymphedema occurs as a result of lymphatic vessel damage or obstruction, leading to the lymphatic fluid stasis, which triggers inflammation, tissue fibrosis, and adipose tissue deposition with adipocyte hypertrophy. The treatment of lymphedema is divided into conservative and surgical approaches. Among surgical treatments, methods like lymphaticovenular anastomosis and vascularized lymph node transfer are gaining attention as they focus on restoring lymphatic flow, constituting a physiologic treatment approach. Lymphatic endothelial cells form the structure of lymphatic vessels. These cells possess button-like junctions that facilitate the influx of fluid and leukocytes. Approximately 10% of interstitial fluid is connected to venous return through lymphatic capillaries. Damage to lymphatic vessels leads to lymphatic fluid stasis, resulting in the clinical condition of lymphedema through three mechanisms: Inflammation involving CD4+ T cells as the principal contributing factor, along with the effects of immune cells on the VEGF-C/VEGFR axis, consequently resulting in abnormal lymphangiogenesis; adipocyte hypertrophy and adipose tissue deposition regulated by the interaction of CCAAT/enhancer-binding protein α and peroxisome proliferator-activated receptor-γ; and tissue fibrosis initiated by the overactivity of Th2 cells, leading to the secretion of profibrotic cytokines such as IL-4, IL-13, and the growth factor TGF-β1. Surgical treatments aimed at reconstructing the lymphatic system help facilitate lymphatic fluid drainage, but their effectiveness in treating already damaged lymphatic vessels is limited. Therefore, reviewing the pathophysiology and molecular mechanisms of lymphedema is crucial to complement surgical treatments and explore novel therapeutic approaches.
摘要：
淋巴水肿是由于淋巴管损伤或阻塞而发生的，导致淋巴液淤滞，引发炎症，组织纤维化，和脂肪细胞肥大的脂肪组织沉积。淋巴水肿的治疗分为保守方法和手术方法。在手术治疗中，淋巴静脉吻合术和血管化淋巴结转移术等方法正受到关注，因为它们专注于恢复淋巴流，构成生理治疗方法。淋巴管内皮细胞形成淋巴管结构。这些细胞具有促进流体和白细胞流入的纽扣状连接。大约10％的间质液通过毛细淋巴管与静脉回流相连。淋巴管的损伤导致淋巴液淤滞，通过三种机制导致淋巴水肿的临床状况：以CD4+T细胞为主要因素的炎症，随着免疫细胞对VEGF-C/VEGFR轴的影响，因此导致异常淋巴管生成；CCAAT/增强子结合蛋白α和过氧化物酶体增殖物激活受体γ相互作用调节的脂肪细胞肥大和脂肪组织沉积；以及由Th2细胞过度活性引发的组织纤维化，导致促纤维化细胞因子如IL-4、IL-13和生长因子TGF-β1的分泌。旨在重建淋巴系统的手术治疗有助于促进淋巴液引流，但是它们在治疗已经受损的淋巴管方面的有效性是有限的。因此,回顾淋巴水肿的病理生理学和分子机制对于补充外科治疗和探索新的治疗方法至关重要。
