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More recently, \u2018non-classical\u2019 MRs have been described in kidney cells not associated with electrolyte transport, including mesangial cells and podocytes within the glomerulus. Activation of MRs in these cells appears to lead to glomerular sclerosis. Mechanistically, aldosterone induces excess production of reactive oxygen species (ROS) and oxidative stress in glomerular cells through activation of NADPH oxidase. In mesangial cells, aldosterone also has pro-apoptotic, mitogenic and pro-fibrogenic effects, all of which potentially promote active remodelling and expansion of the mesangium. Although mitochondrial dysfunction seems to mediate the aldosterone-induced mesangial apoptosis, the ROS dependent epithelial growth factor receptor (EGFR) transactivation is probably responsible for aldosterone-induced mesangial mitosis and proliferation. In podocytes, mitochondrial dysfunction elicited by oxidative stress is an early event associated with aldosterone-induced podocyte injury. Both the p38 MAPK (p38 mitogen-activated protein kinase) signalling and the redox-sensitive glycogen synthase kinase (GSK)3\u03b2 pathways are centrally implicated in aldosterone-induced podocyte death. Aldosterone-induced GSK3\u03b2 over-activity could potentially cause hyperphosphorylation and over-activation of putative GSK3\u03b2 substrates, including structural components of the mitochondrial permeability transition (MPT) pore, all of which lead to cell injury and death. Clinically, proteinuria significantly decreases when aldosterone inhibitors are included in the treatment of many glomerular diseases further supporting the view that mineralocorticoids are important players in glomerular pathology.<\/jats:p>","DOI":"10.1042\/cs20140432","type":"journal-article","created":{"date-parts":[[2015,1,27]],"date-time":"2015-01-27T15:47:55Z","timestamp":1422373675000},"page":"527-535","update-policy":"https:\/\/doi.org\/10.1042\/crossmark_policy","source":"Crossref","is-referenced-by-count":27,"title":["Therapeutic targeting of aldosterone: a novel approach to the treatment of glomerular disease"],"prefix":"10.1042","volume":"128","author":[{"given":"Andrew\u00a0S.","family":"Brem","sequence":"first","affiliation":[{"name":"Division of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rujun","family":"Gong","sequence":"additional","affiliation":[{"name":"Division of Kidney Disease and Hypertension, Department of Medicine, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island, U.S.A."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"288","published-online":{"date-parts":[[2015,1,27]]},"reference":[{"key":"2021113010381396100_B1","doi-asserted-by":"publisher","first-page":"368","DOI":"10.1126\/science.121.3141.368","article-title":"Anticortisol action of aldosterone","volume":"121","author":"Selye","year":"1955","journal-title":"Science"},{"key":"2021113010381396100_B2","doi-asserted-by":"publisher","first-page":"611","DOI":"10.1172\/JCI104946","article-title":"The action of aldosterone and related corticosteroids on sodium transport across the toad bladder","volume":"43","author":"Porter","year":"1964","journal-title":"J. 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