Pal Soumiya, Rahman Jenat, Mu Shengyu, Rusch Nancy J, Stolarz Amanda J
Department of Pharmaceutical Sciences, College of Pharmacy, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Department of Pharmacology and Toxicology, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Front Pharmacol. 2022 Mar 4;13:850586. doi: 10.3389/fphar.2022.850586. eCollection 2022.
The lymphatic circulation is an important component of the circulatory system in humans, playing a critical role in the transport of lymph fluid containing proteins, white blood cells, and lipids from the interstitial space to the central venous circulation. The efficient transport of lymph fluid critically relies on the rhythmic contractions of collecting lymph vessels, which function to "pump" fluid in the distal to proximal direction through the lymphatic circulation with backflow prevented by the presence of valves. When rhythmic contractions are disrupted or valves are incompetent, the loss of lymph flow results in fluid accumulation in the interstitial space and the development of lymphedema. There is growing recognition that many pharmacological agents modify the activity of ion channels and other protein structures in lymph muscle cells to disrupt the cyclic contraction and relaxation of lymph vessels, thereby compromising lymph flow and predisposing to the development of lymphedema. The effects of different medications on lymph flow can be understood by appreciating the intricate intracellular calcium signaling that underlies the contraction and relaxation cycle of collecting lymph vessels. For example, voltage-sensitive calcium influx through long-lasting ("L-type") calcium channels mediates the rise in cytosolic calcium concentration that triggers lymph vessel contraction. Accordingly, calcium channel antagonists that are mainstay cardiovascular medications, attenuate the cyclic influx of calcium through L-type calcium channels in lymph muscle cells, thereby disrupting rhythmic contractions and compromising lymph flow. Many other classes of medications also may contribute to the formation of lymphedema by impairing lymph flow as an off-target effect. The purpose of this review is to evaluate the evidence regarding potential mechanisms of drug-related lymphedema with an emphasis on common medications administered to treat cardiovascular diseases, metabolic disorders, and cancer. Additionally, although current pharmacological approaches used to alleviate lymphedema are largely ineffective, efforts are mounting to arrive at a deeper understanding of mechanisms that regulate lymph flow as a strategy to identify novel anti-lymphedema medications. Accordingly, this review also will provide information on studies that have explored possible anti-lymphedema therapeutics.
淋巴循环是人体循环系统的重要组成部分,在将含有蛋白质、白细胞和脂质的淋巴液从组织间隙输送到中央静脉循环中起着关键作用。淋巴液的有效运输严重依赖于集合淋巴管的节律性收缩,其作用是通过淋巴循环将液体从远端向近端“泵”送,而瓣膜的存在可防止逆流。当节律性收缩受到干扰或瓣膜功能不全时,淋巴液流动的丧失会导致组织间隙中液体积聚并引发淋巴水肿。越来越多的人认识到,许多药物会改变淋巴肌细胞中离子通道和其他蛋白质结构的活性,从而破坏淋巴管的周期性收缩和舒张,进而损害淋巴液流动并易引发淋巴水肿。通过了解集合淋巴管收缩和舒张周期所依赖的复杂细胞内钙信号传导,可以理解不同药物对淋巴液流动的影响。例如,通过长效(“L型”)钙通道的电压敏感性钙内流介导了胞质钙浓度的升高,从而触发淋巴管收缩。因此,作为主要心血管药物的钙通道拮抗剂会减弱钙通过淋巴肌细胞中L型钙通道的周期性内流,从而破坏节律性收缩并损害淋巴液流动。许多其他种类的药物也可能作为非靶向效应通过损害淋巴液流动而导致淋巴水肿的形成。本综述的目的是评估有关药物相关性淋巴水肿潜在机制的证据,重点关注用于治疗心血管疾病、代谢紊乱和癌症的常用药物。此外,尽管目前用于缓解淋巴水肿的药理学方法大多无效,但人们正在加大努力,以更深入地了解调节淋巴液流动的机制,作为确定新型抗淋巴水肿药物的策略。因此,本综述还将提供有关探索可能的抗淋巴水肿治疗方法的研究信息。