Analyses of molecular mechanism of hypertensive cardio-renal relationships focusing on post-transcriptional regulations of ion-transporters.

我们的研究揭示了参与“导致盐敏感性高血压的肾小管机制的分子发病机制”的分子的遗传和生物学意义。“肾小管上皮细胞通过紧密连接彼此连接，高度分化，形成胚胎发育的输尿管芽的小管腔。我们的研究迄今为止，肾小管RA系统，ENaC工作在醛固酮敏感的远端小管细胞作为内源性内分泌系统维持稳态。我们已经建立了分子发病机制模型，通过调节钠重吸收维持稳态，并通过其崩溃导致盐敏感性的病理，发展高血压。

Our research revealed the genetic and biological significance of molecules involved in "Molecular pathogenesis of tubular mechanisms leading to salt-sensitive hypertension." Renal tubular epithelial cells, joined by tight junction with each other, were highly differentiated, forming a tubule lumen of the ureteric bud-derived embryologically. Our research to date, a renal tubular RA system, the ENaC working in aldosterone-sensitive distal tubule cell work as endogenous endocrine systems for maintaining homeostatis. We have established molecular pathogenesis models maintaining homeostasis by regulating sodium reabsorption and via its collapse leading to pathology of salt-sensitivity, developing hypertension.