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钙化性主动脉瓣疾病中的巨噬细胞:旁分泌和近分泌疾病驱动因素

Macrophages in Calcific Aortic Valve Disease: Paracrine and Juxtacrine Disease Drivers.

作者信息

Klauzen Polina, Basovich Liubov, Shishkova Daria, Markova Victoria, Malashicheva Anna

机构信息

Laboratory of Regenerative Biomedicine, Institute of Cytology, Russian Academy of Sciences, Saint-Petersburg 194064, Russia.

Department of Experimental Medicine, Research Institute for Complex Issues of Cardiovascular Diseases, Kemerovo 650002, Russia.

出版信息

Biomolecules. 2024 Dec 2;14(12):1547. doi: 10.3390/biom14121547.

Abstract

A significant role in the pathogenesis of CAVD is played by innate immunity cells, such as macrophages. In stenotic valves, macrophages have enhanced inflammatory activity, and the population's balance is shifted toward pro-inflammatory ones. Pro-inflammatory macrophages release cytokines, chemokines, and microRNA, which can directly affect the resident valvular cells and cause valve calcification. In CAVD patients, macrophages may have more pronounced pro-inflammatory properties, enhanced not only by paracrine signals but also by juxtacrine Notch signaling and epigenetic factors, which influence the maturation of macrophages' progenitors. In this review, we observe the accumulated data on the involvement of macrophages in CAVD development via paracrine and juxtacrine interactions.

摘要

先天性免疫细胞,如巨噬细胞,在钙化性主动脉瓣疾病(CAVD)的发病机制中发挥着重要作用。在狭窄瓣膜中,巨噬细胞的炎症活性增强,细胞群体平衡向促炎细胞倾斜。促炎性巨噬细胞释放细胞因子、趋化因子和微小RNA,这些物质可直接影响瓣膜驻留细胞并导致瓣膜钙化。在CAVD患者中,巨噬细胞可能具有更明显的促炎特性,不仅受到旁分泌信号的增强作用,还受到 juxtacrine Notch信号和表观遗传因素的影响,这些因素会影响巨噬细胞祖细胞的成熟。在本综述中,我们观察了巨噬细胞通过旁分泌和juxtacrine相互作用参与CAVD发展的累积数据。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7c74/11673549/2a96308940d4/biomolecules-14-01547-g001.jpg

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