Biochemical events and cytokine interactions linking glucose metabolism to the development of diabetic nephropathy

Kumar Sharma, Fuad N. Ziyadeh

Research output: Contribution to journalArticle

95 Citations (Scopus)

Abstract

The important role of hyperglycemia in the genesis of diabetic renal disease has been strengthened by tissue culture studies, experimental animal models, and clinical trials. A mechanistic understanding of the cellular and biochemical processes that link hyperglycemia with the development of diabetic nephropathy is indispensable for directing the most optimal therapeutic interventions. Likely mediators of the effects of high ambient glucose include activation of the polyol pathway, increased protein kinase C activity, nonenzymatic glycation of circulating or matrix proteins, and/or aberrant synthesis or actions of cytokines and vasomodulatory agents. The latter include anglotensin II, thromboxane, platelet-derived growth factor, endothelins, insulin-like growth factor-1, and transforming growth factor- β. The studies we review here argue strongly in support of the hypothesis that elevated production and/or activity of transforming growth factor-β in the kidney is a final common mediator of diabetic renal hypertrophy and mesangiel matrix expansion.

Original languageEnglish (US)
Pages (from-to)80-92
Number of pages13
JournalSeminars in Nephrology
Volume17
Issue number2
StatePublished - Apr 1 1997
Externally publishedYes

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Diabetic Nephropathies
Transforming Growth Factors
Cytokines
Kidney
Glucose
Hyperglycemia
Biochemical Phenomena
Thromboxanes
Platelet-Derived Growth Factor
Endothelins
Somatomedins
Protein Kinase C
Hypertrophy
Animal Models
Clinical Trials
Proteins
Therapeutics

ASJC Scopus subject areas

  • Nephrology

Cite this

Biochemical events and cytokine interactions linking glucose metabolism to the development of diabetic nephropathy. / Sharma, Kumar; Ziyadeh, Fuad N.

In: Seminars in Nephrology, Vol. 17, No. 2, 01.04.1997, p. 80-92.

Research output: Contribution to journalArticle

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