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 α, regulates renin expression as well as growth and differentiation genes such as c-myc, the authors propose the hypothesis that liver X receptor α 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.
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