卡尔帕因
炎症
甘露糖受体
ABCA1
受体
细胞生物学
化学
巨噬细胞
免疫系统
甘露糖
内化
生物化学
运输机
免疫学
生物
体外
酶
基因
作者
Hui Yang,Chang Liu,Yanjun Wu,Meng Yuan,Jia‐Run Huang,Yuhan Xia,Qinjie Ling,Peter R. Hoffmann,Zhi Huang,Tianfeng Chen
出处
期刊:Nano Today
[Elsevier]
日期:2021-12-06
卷期号:42: 101351-101351
被引量:36
标识
DOI:10.1016/j.nantod.2021.101351
摘要
Atherosclerosis is a leading cause of death worldwide as characterized by the accumulation of lipid-overloaded macrophages exhibiting high expression of mannose receptors (MRs) in the arterial wall. Hyperactivation of the calpain proteolytic system has been reported to contribute to the progression of atherosclerosis through cleavage of ATP-binding cassette transporter A1 (ABCA1) and G1 (ABCG1) in macrophages. However, the efficiency and specificity of conventional calpain inhibitors are substantially limited, reducing their capacity to influence calpain mediated pathology. To address this issue, a translational nanosystem was developed using immune enhancing selenium in the form of D-mannose modified selenium nanoparticle (MSeNP) loaded with calpain inhibitory peptide (CIP) ([email protected]). The D-mannose modification enhanced accumulation of [email protected] in the atherosclerotic plaques by specifically binding to mannose receptors, thus reducing plaque formation via inhibition of calpain activity, leading to lower levels of atherosclerosis in apolipoprotein E-deficient (ApoE-/-) mice. Moreover, by regulating the ratio of M1/M2 macrophages, [email protected] exhibits strong anti-inflammatory effects. Taken together, this study provides the framework for a targeted nanotherapy to mitigate atherogenesis.
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