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JAHA:循环S‐谷胱甘肽化的cMyBP‐C作为心脏舒张功能障碍的生物标志物

2022-06-07 MedSci原创 MedSci原创

伴有舒张功能障碍的人类、猴子和小鼠循环中S-谷胱甘肽化的cMyBP-C水平升高。S-谷胱甘肽化的cMyBP-C可能是舒张功能障碍新的生物标志物。

射血分数保留的心力衰竭(HFpEF)占心力衰竭患者的50%以上,心脏舒张功能障碍是大多数HFpEF患者的病理表现。近年来,HFpEF的患病率正在增加,导致这类患者的发病率和死亡率也不断增加。但是,目前很少有药理学方法能有效治疗HFpEF。心脏肌球蛋白结合蛋白-C(cMyBP-C)在肌节的组装和稳定中起主要的结构性作用,研究报道cMyBP-C具有调节心脏收缩和舒张的功能。此前,研究人员通过动物模型证明了升高的心肌S-谷胱甘肽化的cMyBP-C与舒张功能障碍相关。

近日,心血管疾病领域权威杂志JAHA上发表了一篇研究文章,在这项研究中,研究人员旨在评估循环S-谷胱甘肽化的cMyBP-C是否可成为舒张功能障碍的生物标志物。

研究人员通过超声心动图确定了人类、非洲绿猴和小鼠的舒张功能障碍,并采集了血样,进行免疫沉淀分析了S-谷胱甘肽化的cMyBP-C水平。与非舒张功能障碍对照组(n=13)相比,患有舒张功能障碍的参与者(n=24)循环中S-谷胱甘肽化的cMyBP-C水平升高(1.46±0.13倍,P=0.014)。

同样,舒张功能障碍的猴子(n=6)循环中S-谷胱甘肽化的cMyBP-C水平也显著升高,约2.13±0.47倍(P=0.047),而伴有舒张功能障碍的小鼠(n=5)升高约1.49(1.22-2.06)倍(P=0.031),相比于各自的非舒张功能障碍对照者。循环中S-谷胱甘肽化的cMyBP-C水平与人类舒张功能障碍严重程度呈正相关。

由此可见,伴有舒张功能障碍的人类、猴子和小鼠循环中S-谷胱甘肽化的cMyBP-C水平升高。S-谷胱甘肽化的cMyBP-C可能是舒张功能障碍新的生物标志物。

原始出处:

Xiaoxu Zhou.et al.Circulating S‐Glutathionylated cMyBP‐C as a Biomarker for Cardiac Diastolic Dysfunction.JAHA.2022.https://www.ahajournals.org/doi/10.1161/JAHA.122.025295

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    2023-04-06 yahu
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    2022-06-08 zhaohui6731
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