3.9 Article

Molecular mechanism of juxtaglomerular cell hyperplasia: a unifying hypothesis

Journal

JOURNAL OF THE AMERICAN SOCIETY OF HYPERTENSION
Volume 1, Issue 3, Pages 164-168

Publisher

ELSEVIER SCIENCE INC
DOI: 10.1016/j.jash.2007.02.004

Keywords

Renin; juxtaglomerular apparatus; gene expression; gene regulation

Funding

  1. National Heart, Lung, and Blood Institute [R01 HL35610, HL58516, HL72010, HL73219]
  2. Edna Mandel Foundation

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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. (C) 2007 American Society of Hypertension. All rights reserved.

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