Meinel S, Gekle M, Grossmann C
Julius Bernstein Institute of Physiology, Martin Luther University Halle-Wittenberg, Germany.
Julius Bernstein Institute of Physiology, Martin Luther University Halle-Wittenberg, Germany.
Steroids. 2014 Dec;91:3-10. doi: 10.1016/j.steroids.2014.05.017. Epub 2014 Jun 11.
The mineralocorticoid receptor (MR) belongs to the steroid receptor superfamily. Classically, it acts as a ligand-bound transcription factor in epithelial tissues, where it regulates water and electrolyte homeostasis and controls blood pressure. Additionally, the MR has been shown to elicit pathophysiological effects including inflammation, fibrosis and remodeling processes in the cardiovascular system and the kidneys and MR antagonists have proven beneficial for patients with certain cardiovascular and renal disease. The underlying molecular mechanisms that mediate MR effects have not been fully elucidated but very likely rely on interactions with other signaling pathways in addition to genomic actions at hormone response elements. In this review we will focus on interactions of MR signaling with different membrane receptors, namely receptor tyrosine kinases and the angiotensin II receptor because of their potential relevance for disease. In addition, GPR30 is discussed as a new aldosterone receptor. To gain insights into the problem why the MR only seems to mediate pathophysiological effects in the presence of additional permissive factors we will also briefly discuss factors that lead to modulation of MR activity as well. Overall, MR signaling is part of an intricate network that still needs to be investigated further.
盐皮质激素受体(MR)属于类固醇受体超家族。传统上,它在上皮组织中作为一种与配体结合的转录因子发挥作用,在该组织中调节水和电解质平衡并控制血压。此外,已证明MR会引发病理生理效应,包括心血管系统和肾脏中的炎症、纤维化和重塑过程,并且MR拮抗剂已被证明对某些心血管和肾脏疾病患者有益。介导MR效应的潜在分子机制尚未完全阐明,但很可能除了在激素反应元件上的基因组作用外,还依赖于与其他信号通路的相互作用。在本综述中,由于其与疾病的潜在相关性,我们将重点关注MR信号通路与不同膜受体(即受体酪氨酸激酶和血管紧张素II受体)的相互作用。此外,GPR30作为一种新的醛固酮受体也将被讨论。为了深入了解为什么MR似乎仅在存在其他许可因子的情况下才介导病理生理效应这一问题,我们还将简要讨论导致MR活性调节的因素。总体而言,MR信号通路是一个仍需进一步研究的复杂网络的一部分。