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Combined AGE inhibition and ACEi decreases the progression of established diabetic nephropathy in B6 db/db mice

Kidney international, 2006-08, Vol.70 (3), p.507-514

2006

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Glomerulosclerosis is transmitted by bone marrow-derived mesangial cell progenitors

The Journal of clinical investigation, 2001-12, Vol.108 (11), p.1649-1656

2001

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Pathogenic effects of advanced glycosylation: biochemical, biologic, and clinical implications for diabetes and aging

Laboratory investigation, 1994-02, Vol.70 (2), p.138

1994

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IGF-1 decreases collagen degradation in diabetic NOD mesangial cells: implications for diabetic nephropathy

Diabetes (New York, N.Y.), 1999-08, Vol.48 (8), p.1638-1644

1999

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Receptor-Specific Increase in Extracellular Matrix Production in Mouse Mesangial Cells by Advanced Glycosylation End Products is Mediated Via Platelet-Derived Growth Factor

Proceedings of the National Academy of Sciences - PNAS, 1992-04, Vol.89 (7), p.2873-2877

1992

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Advanced Glycation End Products Induce Glomerular Sclerosis and Albuminuria in Normal Rats

Proceedings of the National Academy of Sciences - PNAS, 1994-11, Vol.91 (24), p.11704-11708

1994

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Advanced glycation end products up-regulate gene expression found in diabetic glomerular disease

Proceedings of the National Academy of Sciences - PNAS, 1994-09, Vol.91 (20), p.9436-9440

1994

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Strain differences rather than hyperglycemia determine the severity of glomerulosclerosis in mice

Kidney international, 1998-12, Vol.54 (6), p.1999-2007

1998

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Expression and regulation of estrogen receptors in mesangial cells : Influence on matrix metalloproteinase-9

Journal of the American Society of Nephrology, 2001-02, Vol.12 (2), p.241-251

2001

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Nature and Severity of the Glomerular Response to Nephron Reduction Is Strain-Dependent in Mice

The American journal of pathology, 1999-03, Vol.154 (3), p.891-897

1999

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Glomerular mRNAs in human type 1 diabetes: Biochemical evidence for microalbuminuria as a manifestation of diabetic nephropathy

Kidney international, 2001-12, Vol.60 (6), p.2330-2336

2001

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Analysis of Glomerulosclerosis and Atherosclerosis in Lecithin Cholesterol Acyltransferase-deficient Mice

The Journal of biological chemistry, 2001-05, Vol.276 (18), p.15090-15098

2001

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Lupus nephritis: a clinical review for practicing nephrologists

Clinical nephrology, 2002-02, Vol.57 (2), p.95-107

2002

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Mesangial cell turnover: effect of heparin and peptide growth factors

Laboratory investigation, 1991-04, Vol.64 (4), p.446

1991

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Transforming growth factor-beta. Murine glomerular receptors and responses of isolated glomerular cells

The Journal of clinical investigation, 1989-04, Vol.83 (4), p.1160-1167

1989

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Progressive glomerulosclerosis develops in transgenic mice chronically expressing growth hormone and growth hormone releasing factor but not in those expressing insulinlike growth factor-1

The American journal of pathology, 1988-06, Vol.131 (3), p.398-403

1988

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Hepatocyte Growth Factor, but Not Insulin-Like Growth Factor I, Protects Podocytes against Cyclosporin A-Induced Apoptosis

The American journal of pathology, 2001, Vol.158 (1), p.275-280

2001

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Glomerular cell culture

Laboratory investigation, 1985-08, Vol.53 (2), p.122

1985

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Glomerular lesions in mice transgenic for growth hormone and insulinlike growth factor-I. I. Relationship between increased glomerular size and mesangial sclerosis

The American journal of pathology, 1990-09, Vol.137 (3), p.541-552

1990

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Administration of AGEs in vivo induces extracellular matrix gene expression

Nephrology, dialysis, transplantation, 1996, Vol.11 (supp5), p.62-65

1996

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The inheritance of glomerulosclerosis in mice is controlled by multiple quantitative trait loci

Nephrology, dialysis, transplantation, 1998-12, Vol.13 (12), p.3074-3078

1998

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Dissociation of glomerular hypertrophy, cell proliferation, and glomerulosclerosis in mouse strains heterozygous for a mutation (Os) which induces a 50% reduction in nephron number

The Journal of clinical investigation, 1996-03, Vol.97 (5), p.1242-1249

1996

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TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells

American Journal of Physiology: Cell Physiology, 1996-06, Vol.270 (6), p.C1595-C1601

1996

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Protection against diabetes-induced nephropathy in growth hormone receptor/binding protein gene-disrupted mice

Endocrinology (Philadelphia), 2000-01, Vol.141 (1), p.163-168

2000

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Mesangial cells from transgenic mice with progressive glomerulosclerosis exhibit stable, phenotypic changes including undetectable MMP-9 and increased type IV collagen

Laboratory investigation, 1996-12, Vol.75 (6), p.791

1996

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Combined AGE inhibition and ACEi decreases the progression of established diabetic nephropathy in B6 db/db mice

Glomerulosclerosis is transmitted by bone marrow-derived mesangial cell progenitors

Pathogenic effects of advanced glycosylation: biochemical, biologic, and clinical implications for diabetes and aging

IGF-1 decreases collagen degradation in diabetic NOD mesangial cells: implications for diabetic nephropathy

Receptor-Specific Increase in Extracellular Matrix Production in Mouse Mesangial Cells by Advanced Glycosylation End Products is Mediated Via Platelet-Derived Growth Factor

Advanced Glycation End Products Induce Glomerular Sclerosis and Albuminuria in Normal Rats

Advanced glycation end products up-regulate gene expression found in diabetic glomerular disease

Strain differences rather than hyperglycemia determine the severity of glomerulosclerosis in mice

Expression and regulation of estrogen receptors in mesangial cells : Influence on matrix metalloproteinase-9

Nature and Severity of the Glomerular Response to Nephron Reduction Is Strain-Dependent in Mice

Glomerular mRNAs in human type 1 diabetes: Biochemical evidence for microalbuminuria as a manifestation of diabetic nephropathy

Analysis of Glomerulosclerosis and Atherosclerosis in Lecithin Cholesterol Acyltransferase-deficient Mice

Lupus nephritis: a clinical review for practicing nephrologists

Mesangial cell turnover: effect of heparin and peptide growth factors

Transforming growth factor-beta. Murine glomerular receptors and responses of isolated glomerular cells

Progressive glomerulosclerosis develops in transgenic mice chronically expressing growth hormone and growth hormone releasing factor but not in those expressing insulinlike growth factor-1

Hepatocyte Growth Factor, but Not Insulin-Like Growth Factor I, Protects Podocytes against Cyclosporin A-Induced Apoptosis

Glomerular cell culture

Glomerular lesions in mice transgenic for growth hormone and insulinlike growth factor-I. I. Relationship between increased glomerular size and mesangial sclerosis

Administration of AGEs in vivo induces extracellular matrix gene expression

The inheritance of glomerulosclerosis in mice is controlled by multiple quantitative trait loci

Dissociation of glomerular hypertrophy, cell proliferation, and glomerulosclerosis in mouse strains heterozygous for a mutation (Os) which induces a 50% reduction in nephron number

TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells

Protection against diabetes-induced nephropathy in growth hormone receptor/binding protein gene-disrupted mice

Mesangial cells from transgenic mice with progressive glomerulosclerosis exhibit stable, phenotypic changes including undetectable MMP-9 and increased type IV collagen

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