Identification of a novel therapeutic target in vascular dysfunction: a showcase of reverse and forward translational research linking bench to bedside
Identification of a novel therapeutic target in vascular dysfunction: a showcase of reverse and forward translational research linking bench to bedside
复制标题
识别血管功能障碍的新治疗靶点：展示将实验台与床边连接起来的反向和正向转化研究
DOI：
10.1093/eurheartj/ehab263
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发表时间：
2022
影响因子：
39.3
通讯作者：
Minamino Tohru
中科院分区：
文献类型：
--
作者：
Iwata Hiroshi;Minamino Tohru
病理性血管重塑导致血管功能障碍、新生内膜增厚和动脉粥样硬化，其机制复杂，涉及多种细胞，如内皮细胞、血管平滑肌细胞、免疫细胞、成纤维细胞和间充质干细胞。作为这些病理过程的第一步，许多研究都集中在内皮功能障碍的生物学上。1一氧化氮(NO)是一种重要的内皮细胞衍生的血管松弛分子，它的发现和认识到内皮细胞不是分隔血流和血管壁的简单边界后，血管生物学领域取得了重大进展。许多研究也集中在血管重塑中VSMCs的作用，因为这些细胞不仅在缩小管腔和减少周围组织的灌注量方面起着关键作用，而且在斑块中也起着关键作用。
Pathological vascular remodelling, which leads to vascular malfunction, neointima thickening, and atherosclerosis, is governed by complex mechanisms that involve various types of cells, such as endothelial cells, vascular smooth muscle cells (VSMCs), immune cells, fibroblasts, and mesenchymal stem cells. Many investigations have focused on the biology of endothelial dysfunction as an initial step of these pathological processes. 1 After the discovery of nitric oxide (NO), a pivotal endothelium-derived molecule for vascular relaxation, and the recognition that the endothelium is not a simple border dividing the blood stream and the vessel wall, significant progress was made in the field of vascular biology. A number of studies also focused on a role of VSMCs in vascular remodelling because these cells are critically involved not only in narrowing the lumen and decreasing the perfusion of peripheral tissues but also in plaque