Sexual Dimorphism of Corticosteroid Signaling during Kidney Development

Abstract

Sexual dimorphism involves differences between biological sexes that go beyond sexual characteristics. In mammals, differences between sexes have been demonstrated regarding various biological processes, including blood pressure and predisposition to develop hypertension early in adulthood, which may rely on early events during development and in the neonatal period. Recent studies suggest that corticosteroid signaling pathways (comprising glucocorticoid and mineralocorticoid signaling pathways) have distinct tissue-specific expression and regulation during this specific temporal window in a sex-dependent manner, most notably in the kidney. This review outlines the evidence for a gender differential expression and activation of renal corticosteroid signaling pathways in the mammalian fetus and neonate, from mouse to human, that may favor mineralocorticoid signaling in females and glucocorticoid signaling in males. Determining the effects of such differences may shed light on short term and long term pathophysiological consequences, markedly for males.

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The invention of aldosterone, how the past resurfaces in pediatric endocrinology

“…The Serum and glucocorticoid-regulated kinase 1 (sgk1) is the most studied aldosterone-stimulated gene in epithelial tissues, which phosphorylates the ubiquitin ligase Nedd4-2, which in turn controls the retrieval of the subunits of ENaC from the apical membrane of the cell. Several other target genes have been identified such as the Glucocorticoid-Induced Leucine Zipper protein (GILZ), the serine/threonine kinase KS-WNK1 (With No lysine K kinase), the N-myc Down-Regulated Gene 2 (NDRG2), or the small monomeric GTP-binding protein Kirsten Ras (Ki-Ras), which also seem to play pivotal roles during the early phase of aldosterone responses in the nephron (Viengchareun et al, 2007;Laulhé et al, 2021). The PER1 gene has recently been identified as another aldosterone-target gene in the kidney (Gumz et al, 2009), suggesting that aldosterone may also regulate the…”