Regulation of cellular function by mineralocorticoid receptors

Abstract

The mineralocorticoid receptor (MR), activated by aldosterone, influences renal physiology and also contributes to aging and cardiovascular pathology. This thesis investigates how MR activation alters cellular function, focusing on metabolic shifts, ER stress, autophagy, and cell death in an inducible HEK-MR model. Aldosterone stimulation increased glycolysis and triggered stress-response pathways. PDK4 was identified as an MR-target gene potentially involved in glucose metabolism and stress adaptation. Additionally, nitrosative stress enhanced MR translocation and induced the expression of genes associated with cardiac disease. These findings suggest elevated MR activity drives cellular changes contributing to MR-related pathophysiology