TWEAK/Fn14 system and crescent formation in IgA nephropathy
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[1] M. Sánchez-Niño,et al. Non-canonical NFκB activation promotes chemokine expression in podocytes , 2016, Scientific Reports.
[2] Shao-Cong Sun,et al. NF-κB in inflammation and renal diseases , 2015, Cell & Bioscience.
[3] Yusuke Suzuki,et al. Proposal of remission criteria for IgA nephropathy , 2014, Clinical and Experimental Nephrology.
[4] L. Morando,et al. Validation of the Oxford classification of IgA nephropathy in cohorts with different presentations and treatments , 2014, Kidney international.
[5] M. Sánchez-Niño,et al. TWEAK and the progression of renal disease: clinical translation. , 2014, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[6] A. Ramos,et al. Tumor necrosis factor-like weak inducer of apoptosis (TWEAK) and kidney disease , 2014, Current opinion in nephrology and hypertension.
[7] M. Sánchez-Niño,et al. Fn14 in podocytes and proteinuric kidney disease. , 2013, Biochimica et biophysica acta.
[8] Yusuke Suzuki,et al. A histologic classification of IgA nephropathy for predicting long-term prognosis: emphasis on end-stage renal disease. , 2013, Journal of nephrology.
[9] Y. Tomino,et al. Relationships between levels of urinary podocalyxin, number of urinary podocytes, and histologic injury in adult patients with IgA nephropathy. , 2012, Clinical journal of the American Society of Nephrology : CJASN.
[10] M. Sánchez-Niño,et al. TWEAK (tumor necrosis factor-like weak inducer of apoptosis) activates CXCL16 expression during renal tubulointerstitial inflammation. , 2012, Kidney international.
[11] P. Mundel,et al. Cell biology and pathology of podocytes. , 2012, Annual review of physiology.
[12] U. Berg,et al. Predictors of outcome in paediatric IgA nephropathy with regard to clinical and histopathological variables (Oxford classification). , 2012, Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association.
[13] T. Ninomiya,et al. Validation study of oxford classification of IgA nephropathy: the significance of extracapillary proliferation. , 2011, Clinical journal of the American Society of Nephrology : CJASN.
[14] M. Sánchez-Niño,et al. TWEAK, a multifunctional cytokine in kidney injury. , 2011, Kidney international.
[15] Su-xia Wang,et al. Pathologic predictors of renal outcome and therapeutic efficacy in IgA nephropathy: validation of the oxford classification. , 2011, Clinical journal of the American Society of Nephrology : CJASN.
[16] B. Julian,et al. Validation of the Oxford classification of IgA nephropathy. , 2011, Kidney international.
[17] M. Sánchez-Niño,et al. The inflammatory cytokines TWEAK and TNFα reduce renal klotho expression through NFκB. , 2011, Journal of the American Society of Nephrology : JASN.
[18] J. Carrero,et al. Soluble TWEAK plasma levels as a novel biomarker of endothelial function in patients with chronic kidney disease. , 2009, Clinical journal of the American Society of Nephrology : CJASN.
[19] B. Rovin,et al. Urinary TWEAK as a biomarker of lupus nephritis: a multicenter cohort study , 2009, Arthritis research & therapy.
[20] Sandrine Florquin,et al. The Oxford classification of IgA nephropathy: rationale, clinicopathological correlations, and classification. , 2009, Kidney international.
[21] Fernand,et al. The Oxford classification of IgA nephropathy: pathology definitions, correlations, and reproducibility. , 2009, Kidney international.
[22] G. Camussi,et al. Effect of the Monocyte Chemoattractant Protein-1/CC Chemokine Receptor 2 System on Nephrin Expression in Streptozotocin-Treated Mice and Human Cultured Podocytes , 2009, Diabetes.
[23] C. Chung,et al. The monocyte chemoattractant protein-1/CCR2 loop, inducible by TGF-beta, increases podocyte motility and albumin permeability. , 2009, American journal of physiology. Renal physiology.
[24] Yasuhiko Tomino,et al. Revised equations for estimated GFR from serum creatinine in Japan. , 2009, American journal of kidney diseases : the official journal of the National Kidney Foundation.
[25] Irene Jarchum,et al. TNF-like weak inducer of apoptosis (TWEAK) induces inflammatory and proliferative effects in human kidney cells. , 2009, Cytokine.
[26] J. Winkles. The TWEAK–Fn14 cytokine–receptor axis: discovery, biology and therapeutic targeting , 2008, Nature Reviews Drug Discovery.
[27] M. Sánchez-Niño,et al. The cytokine TWEAK modulates renal tubulointerstitial inflammation. , 2008, Journal of the American Society of Nephrology : JASN.
[28] Y. Sado,et al. Podocytes contribute to the formation of glomerular crescents. , 2008, Journal of the American Society of Nephrology : JASN.
[29] Yusuke Suzuki,et al. Amelioration of crescentic glomerulonephritis by RhoA kinase inhibitor, Fasudil, through podocyte protection and prevention of leukocyte migration. , 2008, The American journal of pathology.
[30] P. Dentelli,et al. The monocyte chemoattractant protein-1/cognate CC chemokine receptor 2 system affects cell motility in cultured human podocytes. , 2007, The American journal of pathology.
[31] S. Shankland,et al. Podocytes in culture: past, present, and future. , 2007, Kidney international.
[32] B. Rovin,et al. Urinary TWEAK and the activity of lupus nephritis. , 2006, Journal of autoimmunity.
[33] M. Sánchez-Niño,et al. Cytokine cooperation in renal tubular cell injury: the role of TWEAK. , 2006, Kidney international.
[34] P. Tipping,et al. T cells in crescentic glomerulonephritis. , 2006, Journal of the American Society of Nephrology : JASN.
[35] Yasuhiko Tomino,et al. Synaptopodin orchestrates actin organization and cell motility via regulation of RhoA signalling , 2006, Nature Cell Biology.
[36] R Nair,et al. Is IgA nephropathy the commonest primary glomerulopathy among young adults in the USA? , 2006, Kidney international.
[37] C. Putterman,et al. Proinflammatory Effects of Tweak/Fn14 Interactions in Glomerular Mesangial Cells1 , 2006, The Journal of Immunology.
[38] P. Bruneval,et al. Podocyte involvement in human immune crescentic glomerulonephritis. , 2005, Kidney international.
[39] W. Kriz,et al. Pathways to nephron loss starting from glomerular diseases-insights from animal models. , 2005, Kidney international.
[40] Kevin V Lemley,et al. Podocytopenia and disease severity in IgA nephropathy. , 2002, Kidney international.
[41] C. Smith,et al. A novel TNF receptor family member binds TWEAK and is implicated in angiogenesis. , 2001, Immunity.
[42] S. Thorgeirsson,et al. The Fn14 immediate-early response gene is induced during liver regeneration and highly expressed in both human and murine hepatocellular carcinomas. , 2000, The American journal of pathology.
[43] Y. Hsu,et al. TWEAK, a New Secreted Ligand in the Tumor Necrosis Factor Family That Weakly Induces Apoptosis* , 1997, The Journal of Biological Chemistry.
[44] G. D'Amico,et al. The commonest glomerulonephritis in the world: IgA nephropathy. , 1987, The Quarterly journal of medicine.
[45] M. Uhlén,et al. Neuronal proteins are novel components of podocyte major processes and their expression in glomerular crescents supports their role in crescent formation. , 2013, Kidney international.
[46] J. Carrero,et al. Additive effects of soluble TWEAK and inflammation on mortality in hemodialysis patients. , 2009, Clinical journal of the American Society of Nephrology : CJASN.
[47] J. Davin. Pathogenesis of IgA nephropathy. , 1995, Acta clinica Belgica.
[48] P. Zucchelli,et al. [IgA nephropathy]. , 1985, Medicina clinica.