New mechanism of elevated CA125 in heart failure: The mechanical stress and inflammatory stimuli initiate CA125 synthesis
New mechanism of elevated CA125 in heart failure: The mechanical stress and inflammatory stimuli initiate CA125 synthesis
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心力衰竭中CA125升高的新机制：机械应力和炎症刺激启动CA125合成
DOI：
10.1016/j.mehy.2012.05.042
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发表时间：
2012-09-01
影响因子：
4.7
通讯作者：
Huang, Hui
中科院分区：
文献类型：
--
作者：
Huang, Feifei;Chen, Jie;Huang, Hui
碳水化合物抗原125已知为膜相关粘蛋白。它已被用作肿瘤标志物，可能在一些卵巢癌或其他良性疾病患者的血液中升高。最近，增加血清碳水化合物抗原125水平已被证明在心力衰竭患者。然而，很少有人知道的病理生理机制。已经发现碳水化合物抗原125将响应于机械应力如流体过载和炎症刺激而从间皮细胞表面脱落。高糖链抗原125水平与心力衰竭患者血清中TNF-α、IL-6和IL-10水平呈正相关。这导致提出的假设，即机械应力和炎症刺激都启动碳水化合物抗原125的合成。这一发现表明，糖链抗原125可能是一个有前途的生物标志物，以评估心力衰竭的危险分层和监测治疗过程。(C)2012爱思唯尔有限公司保留所有权利。
Carbohydrate antigen 125 has been known as a membrane-associated mucin. It has found application as a tumor marker that may be elevated in the blood of some patients with ovarian cancer, or other benign conditions. Recently, increased serum carbohydrate antigen 125 levels have been documented in patients with heart failure. However, little is known about the pathophysiologic mechanism. It has been found that carbohydrate antigen 125 will be shed from surfaces of mesothelial cells in response to mechanical stress such as fluid overload, and inflammatory stimuli. High carbohydrate antigen 125 levels are closely related to the presence of serosal fluid and positively correlated with serum TNF-alpha, IL-6 and IL-10 levels in heart failure patients. This leads to proposed hypothesis that the mechanical stress and inflammatory stimuli both initiate carbohydrate antigen 125 synthesis. This finding suggests that carbohydrate antigen 125 might be a promising biomarker to evaluate the risk stratification of heart failure and monitor the process of therapy. (C) 2012 Elsevier Ltd. All rights reserved.