title: Renin-angiotensin system within the diabetic podocyte.
abstract: Diabetic kidney disease is the leading cause of end-stage renal disease. Podocytes are differentiated cells necessary for the development and maintenance of the glomerular basement membrane and the capillary tufts, as well as the function of the glomerular filtration barrier. The epithelial glomerular cells express a local renin-angiotensin system (RAS) that varies in different pathological situations such as hyperglycemia or mechanical stress. RAS components have been shown to be altered in diabetic podocytopathy, and their modulation may modify diabetic nephropathy progression. Podocytes are a direct target for angiotensin II-mediated injury by altered expression and distribution of podocyte proteins. Furthermore, angiotensin II promotes podocyte injury indirectly by inducing cellular hypertrophy, increased apoptosis, and changes in the anionic charge of the glomerular basement membrane, among other effects. RAS blockade has been shown to decrease the level of proteinuria and delay the progression of chronic kidney disease. This review summarizes the local intraglomerular RAS and its imbalance in diabetic podocytopathy. A better understanding of the intrapodocyte RAS might provide a new approach for diabetic kidney disease treatment.
authors.affiliation: Department of Nephrology, Hospital del Mar, Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain; and.
authors.forename: Eva
authors.initials: E
authors.lastname: Márquez
authors.affiliation: Department of Nephrology, Hospital del Mar, Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain; and Red de Investigación Renal (REDINREN), Instituto Carlos III, Madrid, Spain.
authors.forename: Marta
authors.initials: M
authors.lastname: Riera
authors.affiliation: Department of Nephrology, Hospital del Mar, Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain; and Red de Investigación Renal (REDINREN), Instituto Carlos III, Madrid, Spain.
authors.forename: Julio
authors.initials: J
authors.lastname: Pascual
authors.affiliation: Department of Nephrology, Hospital del Mar, Barcelona, Spain; IMIM (Hospital del Mar Medical Research Institute), Barcelona, Spain; and Red de Investigación Renal (REDINREN), Instituto Carlos III, Madrid, Spain msoler@parcdesalutmar.cat.
authors.forename: María José
authors.initials: MJ
authors.lastname: Soler
mesh_terms: D000804:Angiotensin II / Q000378:metabolism; D057911:Angiotensin Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D000818:Animals; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000378:metabolism*; D006801:Humans; D007328:Insulin / Q000494:pharmacology / Q000627:therapeutic use; D050199:Podocytes / Q000187:drug effects / Q000378:metabolism*; D012084:Renin-Angiotensin System
chemical_list: D057911:Angiotensin Receptor Antagonists; D000806:Angiotensin-Converting Enzyme Inhibitors; D007328:Insulin; D000804:Angiotensin II
keywords: ACE2; angiotensin II; podocytes; renin-angiotensin system