New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy

Frank C. Brosius

doi:10.1007/s11154-008-9100-6

New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy

Frank C. Brosius

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

110 Scopus citations

Abstract

Progression of diabetic nephropathy (DN) is manifested by gradual scarring of both the renal glomerulus and tubulointerstitial region. Over the past several years, the general understanding of the pathogenic factors that lead to renal fibrosis in DN has expanded considerably. In this review, some of the important factors that appear to be involved in driving this fibrosing process are discussed, with special emphasis on newer findings and insights. It is now clear that multiple cell types in the kidney contribute to progressive fibrosis in DN. New concepts about bradykinin, TGF-β and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed.

Original language	English (US)
Pages (from-to)	245-254
Number of pages	10
Journal	Reviews in Endocrine and Metabolic Disorders
Volume	9
Issue number	4
DOIs	https://doi.org/10.1007/s11154-008-9100-6
State	Published - Dec 2008
Externally published	Yes

Keywords

Diabetes
Glomerulus
Kidney
Matrix proteins
Signaling

ASJC Scopus subject areas

Endocrinology, Diabetes and Metabolism
Endocrinology

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10.1007/s11154-008-9100-6

Cite this

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title = "New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy",

abstract = "Progression of diabetic nephropathy (DN) is manifested by gradual scarring of both the renal glomerulus and tubulointerstitial region. Over the past several years, the general understanding of the pathogenic factors that lead to renal fibrosis in DN has expanded considerably. In this review, some of the important factors that appear to be involved in driving this fibrosing process are discussed, with special emphasis on newer findings and insights. It is now clear that multiple cell types in the kidney contribute to progressive fibrosis in DN. New concepts about bradykinin, TGF-β and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed.",

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

author = "Brosius, {Frank C.}",

note = "Funding Information: Acknowledgments Relevant research in Dr. Brosius{\textquoteright} laboratory is supported, in part, by National Institutes of Health grant U01DK076139 and Juvenile Diabetes Research Foundation grant 1-2005-347.",

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doi = "10.1007/s11154-008-9100-6",

language = "English (US)",

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AU - Brosius, Frank C.

N1 - Funding Information: Acknowledgments Relevant research in Dr. Brosius’ laboratory is supported, in part, by National Institutes of Health grant U01DK076139 and Juvenile Diabetes Research Foundation grant 1-2005-347.

PY - 2008/12

Y1 - 2008/12

N2 - Progression of diabetic nephropathy (DN) is manifested by gradual scarring of both the renal glomerulus and tubulointerstitial region. Over the past several years, the general understanding of the pathogenic factors that lead to renal fibrosis in DN has expanded considerably. In this review, some of the important factors that appear to be involved in driving this fibrosing process are discussed, with special emphasis on newer findings and insights. It is now clear that multiple cell types in the kidney contribute to progressive fibrosis in DN. New concepts about bradykinin, TGF-β and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed.

AB - Progression of diabetic nephropathy (DN) is manifested by gradual scarring of both the renal glomerulus and tubulointerstitial region. Over the past several years, the general understanding of the pathogenic factors that lead to renal fibrosis in DN has expanded considerably. In this review, some of the important factors that appear to be involved in driving this fibrosing process are discussed, with special emphasis on newer findings and insights. It is now clear that multiple cell types in the kidney contribute to progressive fibrosis in DN. New concepts about bradykinin, TGF-β and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed.

KW - Diabetes

KW - Glomerulus

KW - Kidney

KW - Matrix proteins

KW - Signaling

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JF - Reviews in Endocrine and Metabolic Disorders

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New insights into the mechanisms of fibrosis and sclerosis in diabetic nephropathy

Abstract

Keywords

ASJC Scopus subject areas

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