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New mechanism of elevated CA125 in heart failure: The mechanical stress and inflammatory stimuli initiate CA125 synthesis

机译:心力衰竭中CA125升高的新机制:机械压力和炎症刺激引发CA125合成

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摘要

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-α, 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.
机译:碳水化合物抗原125被称为膜相关粘蛋白。已经发现它被用作可能在某些患有卵巢癌或其他良性疾病的患者的血液中升高的肿瘤标志物。最近,心力衰竭患者的血清糖类抗原125水平增加。但是,对其病理生理机制知之甚少。已经发现,响应于诸如液体超负荷和炎症刺激的机械应力,碳水化合物抗原125将从间皮细胞的表面脱落。心衰患者中高碳水化合物抗原125水平与浆液的存在密切相关,并且与血清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均引发碳水化合物抗原125的合成。这一发现表明,碳水化合物抗原125可能是一种有前途的生物标志物,可用于评估心力衰竭的风险分层并监测治疗过程。

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