Liao Liwei, Deng Mingming, Gao Qian, Zhang Qin, Bian Yiding, Wang Zilin, Li Jiaye, Xu Weidong, Li Chang, Wang Kai, Zheng Ziwen, Zhou Xiaoming, Hou Gang
National Center for Respiratory Medicine, State Key Laboratory of Respiratory Health and Multimorbidity, National Clinical Research Center for Respiratory Diseases, Institute of Respiratory Medicine, Chinese Academy of Medical Sciences, Department of Pulmonary and Critical Care Medicine, Center of Respiratory Medicine, China-Japan Friendship Hospital, Beijing, China.
Respiratory Department, Center for Pulmonary Vascular Diseases, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing, China.
Int J Biol Macromol. 2024 Aug;275(Pt 2):133741. doi: 10.1016/j.ijbiomac.2024.133741. Epub 2024 Jul 8.
Sarcopenia, characterized by progressive muscle dysfunction, is a common complication of chronic obstructive pulmonary disease (COPD). Our previous study revealed serum Lipoprotein-associated phospholipaseA2 (Lp-PLA2) level significantly increased in COPD and associated with exercise tolerance. This study further investigated the functions and target potential of Lp-PLA2 for sarcopenia in COPD.
The circulating Lp-PLA2 level/enzyme activity in COPD patients and age-matched healthy volunteers were measured. Clinical parameters on skeletal muscle were measured and their correlations with Lp-PLA2 were analyzed. We explored the involvement of Lp-PLA2 in vivo and treatment effectiveness of darapladib (a specific Lp-PLA2 inhibitor) in CS-induced muscle dysfunction models.
Circulating Lp-PLA2 level/enzyme activity was elevated in COPD patients compared with healthy controls, negatively associated with skeletal muscle mass and function. In CS-induced muscle dysfunction murine models, up-regulated serum Lp-PLA2 level/enzyme activity was verified again. In CS-exposed mouse models, darapladib treatment reversed muscle mass loss and muscle dysfunction, meanwhile rescued upregulation of MuRF1 and atrogin-1, and activation of inflammatory factors, oxidant enzymes and NF-κB signaling.
Lp-PLA2 could be a potential indicator for sarcopenia in COPD. Darapladib, a Lp-PLA2 inhibitor, can alleviate CS-induced skeletal muscle dysfunction and represents a potential therapeutic for sarcopenia in COPD.
肌肉减少症以进行性肌肉功能障碍为特征,是慢性阻塞性肺疾病(COPD)的常见并发症。我们之前的研究表明,COPD患者血清脂蛋白相关磷脂酶A2(Lp-PLA2)水平显著升高,并与运动耐力相关。本研究进一步探讨了Lp-PLA2在COPD肌肉减少症中的作用及潜在靶点。
测量COPD患者和年龄匹配的健康志愿者的循环Lp-PLA2水平/酶活性。测量骨骼肌的临床参数,并分析它们与Lp-PLA2的相关性。我们探讨了Lp-PLA2在体内的作用以及达拉匹林(一种特异性Lp-PLA2抑制剂)在香烟烟雾(CS)诱导的肌肉功能障碍模型中的治疗效果。
与健康对照组相比,COPD患者的循环Lp-PLA2水平/酶活性升高,与骨骼肌质量和功能呈负相关。在CS诱导的肌肉功能障碍小鼠模型中,血清Lp-PLA2水平/酶活性再次被证实上调。在暴露于CS的小鼠模型中,达拉匹林治疗可逆转肌肉质量损失和肌肉功能障碍,同时挽救肌肉萎缩相关蛋白1(MuRF1)和肌肉萎缩F-box蛋白1(atrogin-1)的上调以及炎症因子、氧化酶和核因子κB(NF-κB)信号通路的激活。
Lp-PLA2可能是COPD患者肌肉减少症的一个潜在指标。Lp-PLA2抑制剂达拉匹林可减轻CS诱导的骨骼肌功能障碍,是COPD肌肉减少症的一种潜在治疗方法。