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细胞外基质金属蛋白酶诱导因子 EMMPRIN(CD147)与心血管疾病。

Extracellular Matrix Metalloproteinase Inducer EMMPRIN (CD147) in Cardiovascular Disease.

机构信息

Medizinische Klinik III, Kardiologie und Kreislauferkrankungen, Eberhard Karls-Universität Tübingen, 72076 Tübingen, Germany.

Institut für Experimentelle Biomedizin, Universitätsklinikum Würzburg, 97080 Würzburg, Germany.

出版信息

Int J Mol Sci. 2018 Feb 8;19(2):507. doi: 10.3390/ijms19020507.

DOI:10.3390/ijms19020507
PMID:29419744
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5855729/
Abstract

The receptor EMMPRIN is involved in the development and progression of cardiovascular diseases and in the pathogenesis of myocardial infarction. There are several binding partners of EMMPRIN mediating the effects of EMMPRIN in cardiovascular diseases. EMMPRIN interaction with most binding partners leads to disease progression by mediating cytokine or chemokine release, the activation of platelets and monocytes, as well as the formation of monocyte-platelet aggregates (MPAs). EMMPRIN is also involved in atherosclerosis by mediating the infiltration of pro-inflammatory cells. There is also evidence that EMMPRIN controls energy metabolism of cells and that EMMPRIN binding partners modulate intracellular glycosylation and trafficking of EMMPRIN towards the cell membrane. In this review, we systematically discuss these multifaceted roles of EMMPRIN and its interaction partners, such as Cyclophilins, in cardiovascular disease.

摘要

细胞外基质金属蛋白酶诱导因子(EMMPRIN)参与心血管疾病的发生发展和心肌梗死的发病机制。有几种 EMMPRIN 的结合伴侣介导了 EMMPRIN 在心血管疾病中的作用。EMMPRIN 与大多数结合伴侣的相互作用通过介导细胞因子或趋化因子的释放、血小板和单核细胞的激活以及单核细胞-血小板聚集物(MPA)的形成,导致疾病进展。EMMPRIN 还通过介导促炎细胞的浸润参与动脉粥样硬化。也有证据表明,EMMPRIN 控制细胞的能量代谢,EMMPRIN 的结合伴侣调节细胞内糖基化和 EMMPRIN 向细胞膜的运输。在这篇综述中,我们系统地讨论了 EMMPRIN 及其结合伴侣(如亲环素)在心血管疾病中的这些多方面作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/73f5e259f97f/ijms-19-00507-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/13ac4b7c3b1c/ijms-19-00507-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/715b35a601d4/ijms-19-00507-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/17286d66e06f/ijms-19-00507-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/73f5e259f97f/ijms-19-00507-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/13ac4b7c3b1c/ijms-19-00507-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/715b35a601d4/ijms-19-00507-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/17286d66e06f/ijms-19-00507-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b555/5855729/73f5e259f97f/ijms-19-00507-g004.jpg

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