Abnormalities in signaling pathways in diabetic nephropathy

Frank C. Brosius; Charbel C. Khoury; Carolyn L. Buller; Sheldon Chen

doi:10.1586/eem.09.70

Abnormalities in signaling pathways in diabetic nephropathy

Frank C. Brosius, Charbel C. Khoury, Carolyn L. Buller, Sheldon Chen

Research output: Contribution to journal › Review article › peer-review

89 Scopus citations

Abstract

Diabetic nephropathy (DN) is characterized by a plethora of signaling abnormalities that together ultimately result in the clinical and pathologic hallmarks of DN, namely progressive albuminuria followed by a gradual decline in glomerular filtration rate leading to kidney failure, and accompanied by podocyte loss, progressive glomerular sclerosis and, ultimately, progressive tubulointerstitial fibrosis. Over the past few years, the general understanding of the abnormalities in signaling pathways that lead to DN has expanded considerably. In this review, some of the important pathways that appear to be involved in driving this process are discussed, with special emphasis on newer findings and insights. Newer concepts regarding signaling changes in bradykinin, mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated protein C and other pathways are discussed.

Original language	English (US)
Pages (from-to)	51-64
Number of pages	14
Journal	Expert Review of Endocrinology and Metabolism
Volume	5
Issue number	1
DOIs	https://doi.org/10.1586/eem.09.70
State	Published - Jan 2010
Externally published	Yes

Keywords

Diabetes
Glomerulus
Matrix proteins
Signaling

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism

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10.1586/eem.09.70

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title = "Abnormalities in signaling pathways in diabetic nephropathy",

abstract = "Diabetic nephropathy (DN) is characterized by a plethora of signaling abnormalities that together ultimately result in the clinical and pathologic hallmarks of DN, namely progressive albuminuria followed by a gradual decline in glomerular filtration rate leading to kidney failure, and accompanied by podocyte loss, progressive glomerular sclerosis and, ultimately, progressive tubulointerstitial fibrosis. Over the past few years, the general understanding of the abnormalities in signaling pathways that lead to DN has expanded considerably. In this review, some of the important pathways that appear to be involved in driving this process are discussed, with special emphasis on newer findings and insights. Newer concepts regarding signaling changes in bradykinin, mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated protein C and other pathways are discussed.",

keywords = "Diabetes, Glomerulus, Matrix proteins, Signaling",

author = "Brosius, {Frank C.} and Khoury, {Charbel C.} and Buller, {Carolyn L.} and Sheldon Chen",

note = "Funding Information: Relevant research in Frank Brosius{\textquoteright} laboratory was supported, in part, by NIH grant U01DK076139 and R24 R24 DK082841 and in Sheldon Chen{\textquoteright}s laboratory by NIH grant R01DK044513 and a VA Merit Review grant.. �hee authorss havee noo otherr relevantt a��liationss orr �nanciall involve� ment with any organization or entity with a �nancial interest in or �nancial conflict with the subject matter or materials discussed in the manuscript apart �rom those disclosed.",

year = "2010",

month = jan,

doi = "10.1586/eem.09.70",

language = "English (US)",

volume = "5",

pages = "51--64",

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T1 - Abnormalities in signaling pathways in diabetic nephropathy

AU - Brosius, Frank C.

AU - Khoury, Charbel C.

AU - Buller, Carolyn L.

AU - Chen, Sheldon

N1 - Funding Information: Relevant research in Frank Brosius’ laboratory was supported, in part, by NIH grant U01DK076139 and R24 R24 DK082841 and in Sheldon Chen’s laboratory by NIH grant R01DK044513 and a VA Merit Review grant.. �hee authorss havee noo otherr relevantt a��liationss orr �nanciall involve� ment with any organization or entity with a �nancial interest in or �nancial conflict with the subject matter or materials discussed in the manuscript apart �rom those disclosed.

PY - 2010/1

Y1 - 2010/1

N2 - Diabetic nephropathy (DN) is characterized by a plethora of signaling abnormalities that together ultimately result in the clinical and pathologic hallmarks of DN, namely progressive albuminuria followed by a gradual decline in glomerular filtration rate leading to kidney failure, and accompanied by podocyte loss, progressive glomerular sclerosis and, ultimately, progressive tubulointerstitial fibrosis. Over the past few years, the general understanding of the abnormalities in signaling pathways that lead to DN has expanded considerably. In this review, some of the important pathways that appear to be involved in driving this process are discussed, with special emphasis on newer findings and insights. Newer concepts regarding signaling changes in bradykinin, mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated protein C and other pathways are discussed.

AB - Diabetic nephropathy (DN) is characterized by a plethora of signaling abnormalities that together ultimately result in the clinical and pathologic hallmarks of DN, namely progressive albuminuria followed by a gradual decline in glomerular filtration rate leading to kidney failure, and accompanied by podocyte loss, progressive glomerular sclerosis and, ultimately, progressive tubulointerstitial fibrosis. Over the past few years, the general understanding of the abnormalities in signaling pathways that lead to DN has expanded considerably. In this review, some of the important pathways that appear to be involved in driving this process are discussed, with special emphasis on newer findings and insights. Newer concepts regarding signaling changes in bradykinin, mTOR, JAK/STAT, MCP-1, VEGF, endothelial nitric oxide synthase, activated protein C and other pathways are discussed.

KW - Diabetes

KW - Glomerulus

KW - Matrix proteins

KW - Signaling

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DO - 10.1586/eem.09.70

M3 - Review article

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Abnormalities in signaling pathways in diabetic nephropathy

Abstract

Keywords

ASJC Scopus subject areas

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