Angiotensin II-induced podocyte apoptosis is mediated by endoplasmic reticulum stress/PKC-δ/p38 MAPK pathway activation and trough increased Na+/H+ exchanger isoform 1 activity

被引:0
作者
Vanessa Gerolde Cardoso
Guilherme Lopes Gonçalves
Juliana Martins Costa-Pessoa
Karina Thieme
Bruna Bezerra Lins
Fernando Augusto Malavazzi Casare
Mariana Charleaux de Ponte
Niels Olsen Saraiva Camara
Maria Oliveira-Souza
机构
[1] University of Sao Paulo,Laboratory of Renal Physiology, Department of Physiology and Biophysics, Institute of Biomedical Sciences
[2] University of Sao Paulo,Laboratory for Transplantation Immunobiology, Department of Immunology, Institute of Biomedical Sciences
[3] University of Sao Paulo,Laboratory of Carbohydrates and Radioimmunoassays (LIM
来源
BMC Nephrology | / 19卷
关键词
Podocytes; Apoptosis; Angiotensin II; PKC-delta; p38 MAPK; NHE1;
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[1]  
Asanuma K(2003)The role of podocytes in glomerular pathobiology Clin Exp Nephrol 7 255-259
[2]  
Mundel P(2004)Changes in glomerular perm-selectivity induced by angiotensin II imply podocyte dysfunction and slit diaphragm protein rearrangement Semin Nephrol 24 131-140
[3]  
Benigni A(2006)Pathophysiologic implications of reduced podocyte number in a rat model of progressive glomerular injury Am J Pathol 168 42-54
[4]  
Gagliardini E(2006)Podocyte injury and targeting therapy: an update Curr Opin Nephrol Hypertens 15 1-7
[5]  
Remuzzi G(2004)Angiotensin II type 1 receptor overexpression in podocytes induces glomerulosclerosis in transgenic rats J Am Soc Nephrol 15 1475-1487
[6]  
Macconi D(2008)Angiotensin II infusion induces nephrin expression changes and podocyte apoptosis Am J Nephrol 28 500-507
[7]  
Bonomelli M(2016)Renovascular remodeling and renal injury after extended angiotensin II infusion Am J Physiol Renal Physiol 310 F1295-F1307
[8]  
Benigni A(1994)Dysfunctions of cell biological mechanisms of visceral epithelial cell (podocytes) in glomerular diseases Kidney Int 45 300-313
[9]  
Plati T(2001)Apoptosis in podocytes induced by TGF-beta and Smad7 J Clin Invest 108 807-816
[10]  
Sangalli F(2013)AKT2 is essential to maintain podocyte viability and function during chronic kidney disease Nat Med 19 1288-1296