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The antiatherogenic function of kallistatin and its potential mechanism.
Acta Biochimica et Biophysica Sinica ( IF 3.3 ) Pub Date : 2020-05-11 , DOI: 10.1093/abbs/gmaa035
Gang Wang 1 , Jin Zou 1 , Xiaohua Yu 2 , Shanhui Yin 1 , Chaoke Tang 1
Affiliation  

Atherosclerosis is the pathological basis of most cardiovascular diseases, the leading cause of morbidity and mortality worldwide. Kallistatin, originally discovered in human serum, is a tissue-kallikrein-binding protein and a unique serine proteinase inhibitor. Upon binding to its receptor integrin β3, lipoprotein receptor-related protein 6, nucleolin, or Krüppel-like factor 4, kallistatin can modulate various signaling pathways and affect multiple biological processes, including angiogenesis, inflammatory response, oxidative stress, and tumor growth. Circulating kallistatin levels are significantly decreased in patients with coronary artery disease and show an inverse correlation with its severity. Importantly, both in vitro and in vivo experiments have demonstrated that kallistatin reduces atherosclerosis by inhibiting vascular inflammation, antagonizing endothelial dysfunction, and improving lipid metabolism. Thus, kallistatin may be a novel biomarker and a promising therapeutic target for atherosclerosis-related diseases. In this review, we focus on the antiatherogenic function of kallistatin and its potential mechanism.

中文翻译:

利司他汀的抗动脉粥样硬化作用及其潜在机制。

动脉粥样硬化是大多数心血管疾病的病理基础,是全世界发病率和死亡率的主要原因。最初在人血清中发现的Kallistatin是组织激肽释放酶结合蛋白和独特的丝氨酸蛋白酶抑制剂。结合其受体整联蛋白β3,脂蛋白受体相关蛋白6,核仁蛋白或Krüppel样因子4后,kalistlistatin可以调节各种信号传导途径并影响多种生物学过程,包括血管生成,炎症反应,氧化应激和肿瘤生长。冠状动脉疾病患者中的循环钾利司他汀水平显着降低,并与其严重程度呈负相关。重要的是,在体外体内实验证明,他司他汀通过抑制血管炎症,拮抗内皮功能障碍和改善脂质代谢来减少动脉粥样硬化。因此,Kallistatin可能是动脉粥样硬化相关疾病的新型生物标志物和有希望的治疗靶标。在这篇综述中,我们着重于利他汀的抗动脉粥样硬化作用及其潜在机制。
更新日期:2020-07-03
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