Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells.
Signal transduction mechanisms mediating the physiological and pathophysiological actions of angiotensin II in vascular smooth muscle cells.
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DOI：
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发表时间：
2000-12
影响因子：
21.1
通讯作者：
R. Touyz;E. Schiffrin
中科院分区：
文献类型：
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作者：
R. Touyz;E. Schiffrin
直到最近，血管紧张素II(Ang II)在血管平滑肌细胞中引发的信号事件被认为是快速、短暂的，并被划分为不同的线性通路，其中磷脂酶C-二酰甘油-钙(2+)轴的细胞内靶点与酪氨酸激酶和丝裂原激活的蛋白激酶依赖的通路不同。然而，这些主要的细胞内信号级联不是独立发挥作用的，而是积极地参与串扰。来自Ang II结合受体的下游信号汇聚在一起，引发复杂和多重的反应。连接多条细胞内途径的确切适配蛋白或“中间人”分子有待澄清。血管紧张素Ⅱ在不同的组织中诱导多种作用，血管紧张素受体占据和激活后的信号事件受到严格控制和极其复杂。在高血压、动脉粥样硬化和介入术后再狭窄等心血管疾病的血管病理过程中，这些高度调控的信号通路的改变可能在结构和功能异常中起关键作用。
Until recently, the signaling events elicited in vascular smooth muscle cells by angiotensin II (Ang II) were considered to be rapid, short-lived, and divided into separate linear pathways, where intracellular targets of the phospholipase C-diacylglycerol-Ca(2+) axis were distinct from those of the tyrosine kinase- and mitogen-activated protein kinase- dependent pathways. However, these major intracellular signaling cascades do not function independently and are actively engaged in cross-talk. Downstream signals from the Ang II-bound receptors converge to elicit complex and multiple responses. The exact adapter proteins or "go-between" molecules that link the multiple intracellular pathways await clarification. Ang II induces a multitude of actions in various tissues, and the signaling events following occupancy and activation of angiotensin receptors are tightly controlled and extremely complex. Alterations of these highly regulated signaling pathways in vascular smooth cells may be pivotal in structural and functional abnormalities that underlie vascular pathological processes in cardiovascular diseases such as hypertension, atherosclerosis, and post-interventional restenosis.