球旁细胞增生的分子机制：一个统一的假说。

Molecular mechanism of juxtaglomerular cell hyperplasia: a unifying hypothesis.

作者信息

Matsushita Kenichi, Zhang Zhiping, Pratt Richard E, Dzau Victor J

机构信息

Mandel Center for Hypertension Research, Duke University Medical Center, Durham, North Carolina, USA; Cardiology Division, Department of Medicine, Duke University Medical Center, Durham, North Carolina, USA.

出版信息

J Am Soc Hypertens. 2007 May-Jun;1(3):164-8. doi: 10.1016/j.jash.2007.02.004.

DOI:10.1016/j.jash.2007.02.004

PMID:20409848

Abstract

Renin is the first enzymatic step of the renin angiotensin cascade and plays an important role in cardiovascular homeostasis. Renin is mainly expressed in and released from specialized juxtaglomerular (JG) cells in kidney. JG cells develop hyperplasia in response to various chronic stimuli while maintaining the ability to express high levels of renin. However, the molecular and cellular mechanisms of JG cell hyperplasia are unknown. Based on the authors' previous observation that a nuclear hormone receptor, liver X receptor alpha, regulates renin expression as well as growth and differentiation genes such as c-myc, the authors propose the hypothesis that liver X receptor alpha can contribute to JG cell hyperplasia under conditions of chronic and intense induction of these genes. This hypothesis may provide a potential explanation for the observation that the JG cells can maintain a highly specialized renin-producing phenotype while undergoing hyperplasia.

摘要

肾素是肾素-血管紧张素级联反应的首个酶促步骤，在心血管稳态中发挥重要作用。肾素主要在肾脏中特化的球旁（JG）细胞表达并释放。JG细胞在各种慢性刺激下会发生增生，同时保持表达高水平肾素的能力。然而，JG细胞增生的分子和细胞机制尚不清楚。基于作者之前的观察，即核激素受体肝X受体α调节肾素表达以及诸如c-myc等生长和分化基因，作者提出假说：在这些基因受到慢性和强烈诱导的情况下，肝X受体α可能促成JG细胞增生。这一假说可能为JG细胞在增生时能维持高度特化的肾素产生表型这一观察结果提供潜在解释。