title: Podocyte biology in diabetic nephropathy.
abstract: Glomerular visceral epithelial cells, namely podocytes, are highly specialized cells and give rise to primary processes, secondary processes, and finally foot processes. The foot processes of neighboring podocytes interdigitate, leaving between them filtration slits. These are bridged by an extracellular substance, known as the slit diaphragm, which plays a major role in establishing size-selective barrier to protein loss. Furthermore, podocytes are known to synthesize matrix molecules to the glomerular basement membrane (GBM), including type IV collagen, laminin, entactin, and agrin. Because diabetic nephropathy is clinically characterized by proteinuria and pathologically by glomerular hypertrophy and GBM thickening with foot process effacement, podocytes have been the focus in the field of research on diabetic nephropathy. As a result, many investigations have demonstrated that the diabetic milieu per se, hemodynamic changes, and local growth factors such as transforming growth factor-beta and angiotensin II, which are considered mediators in the pathogenesis of diabetic nephropathy, induce directly and/or indirectly hypertrophy, apoptosis, and structural changes, and increase type IV collagen synthesis in podocytes. This review explores some of the structural and functional changes of podocytes under diabetic conditions and their role in the development and progression of diabetic nephropathy.
authors.affiliation: Department of Internal Medicine, Nephrology and Dialysis Unit, The Affiliated Hospital, YanBian University Medical College, JiLin, China.
authors.forename: J J
authors.initials: JJ
authors.lastname: Li
authors.forename: S J
authors.initials: SJ
authors.lastname: Kwak
authors.forename: D S
authors.initials: DS
authors.lastname: Jung
authors.forename: J-J
authors.initials: JJ
authors.lastname: Kim
authors.forename: T-H
authors.initials: TH
authors.lastname: Yoo
authors.forename: D-R
authors.initials: DR
authors.lastname: Ryu
authors.forename: S H
authors.initials: SH
authors.lastname: Han
authors.forename: H Y
authors.initials: HY
authors.lastname: Choi
authors.forename: J E
authors.initials: JE
authors.lastname: Lee
authors.forename: S J
authors.initials: SJ
authors.lastname: Moon
authors.forename: D K
authors.initials: DK
authors.lastname: Kim
authors.forename: D S
authors.initials: DS
authors.lastname: Han
authors.forename: S-W
authors.initials: SW
authors.lastname: Kang
mesh_terms: D049109:Cell Proliferation; D003928:Diabetic Nephropathies / Q000209:etiology / Q000473:pathology / Q000503:physiopathology*; D018450:Disease Progression; D006801:Humans; D006984:Hypertrophy / Q000473:pathology; D007365:Intercellular Junctions / Q000473:pathology / Q000502:physiology; D007678:Kidney Glomerulus / Q000473:pathology / Q000503:physiopathology; D050199:Podocytes / Q000473:pathology* / Q000502:physiology*