Novel Mechanisms for the Control of Renin Synthesis and Release
Novel Mechanisms for the Control of Renin Synthesis and Release
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DOI：
10.1007/s11906-009-0080-z
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发表时间：
2010-02-01
影响因子：
5.6
通讯作者：
Gomez, R. Ariel
中科院分区：
文献类型：
--
作者：
Lopez, Maria Luisa S. Sequeira;Gomez, R. Ariel
肾素是导致血管紧张素生成和控制血压和液体/电解质稳态的酶级联中的关键调节步骤。在成年无应激动物中，肾素由肾肾小球细胞合成和释放。然而，当体内平衡受到威胁时，表达和释放肾素的细胞数量增加并延伸到肾小球区域之外;结果是循环中的肾素增加和体内平衡的重建。肾素细胞数量的增加，称为募集的过程，是通过来源于肾素谱系的细胞中的去分化和再表达来实现的。调节肾素表型的重新获得、肾素合成和肾素释放的相关过程的机制开始被理解。许多研究指出cAMP是调节肾素表型的中心共同因子。此外，我们看到缝隙连接和microRNA的出现，作为更完整地了解肾素细胞复杂调控的新的和有前途的途径。
Renin is the key regulated step in the enzymatic cascade that leads to angiotensin generation and the control of blood pressure and fluid/electrolyte homeostasis. In the adult unstressed animal, renin is synthesized and released by renal juxtaglomerular cells. However, when homeostasis is threatened, the number of cells that express and release renin increases and extends beyond the juxtaglomerular area; the result is an increase in circulating renin and the reestablishment of homeostasis. The increase in the number of renin cells, a process termed recruitment, is achieved by dedifferentiation and re-expression of renin in cells derived from the renin lineage. The mechanisms that regulate the related processes of reacquisition of the renin phenotype, renin synthesis, and renin release are beginning to be understood. Numerous studies point to cAMP as a central common factor for the regulation of renin phenotype. In addition, we are seeing the emergence of gap junctions and microRNAs as new and promising avenues for a more complete understanding of the complex regulation of the renin cell.