Angiotensin II-Induced Signaling Pathways in Diabetes
Autor: | Mario B. Marrero, David Fulton, David M. Stern, David W. Stepp |
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Rok vydání: | 2005 |
Předmět: |
Glycation End Products
Advanced medicine.medical_specialty Vascular smooth muscle Endocrinology Diabetes and Metabolism Glomerular Mesangial Cell Muscle Smooth Vascular Endocrinology Polyol pathway Glycation Internal medicine Diabetes mellitus Diabetes Mellitus Humans Medicine Diabetic Nephropathies business.industry Angiotensin II medicine.disease Glomerular Mesangium Hyperglycemia Cancer research Signal transduction Reactive Oxygen Species business Janus kinase Cell Division Diabetic Angiopathies Signal Transduction |
Zdroj: | Current Diabetes Reviews. 1:197-202 |
ISSN: | 1573-3998 |
DOI: | 10.2174/1573399054022802 |
Popis: | Excessive cellular proliferation is a major contributor to the pathological changes associated with the secondary complications of diabetes. In particular, hyperglycemia (HG)-induced growth of vascular smooth muscle cells (VSMC) and glomerular mesangial cells (GMC) are characteristic features of the cardiovascular and renal complications of diabetes. VSMC and GMC respond to traditional growth factors, however in diabetes this occurs in the context of an environment, enriched in circulating vasoactive mediators and HG. For example, signaling via the angiotensin II (Ang II) pathway has been implicated in the pathogenesis of diabetic vascular disease. Recent findings indicate that HG and Ang II activate intracellular processes, including the polyol pathway and the generation of reactive oxygen species. These pathways activate the JAK (janus kinase)/STAT (signal transducers and activators of transcription) signaling cascades in both VSMC and GMC. Activation of the latter signaling cascade can stimulate excessive proliferation and growth of these cells, contributing to the accelerated atherosclerosis and nephropathy seen in the diabetic state. This review focuses on key factors in the diabetic microenvironment, in particular the interplay between HG, accumulation of advanced glycation end products and Ang II mediated signaling events both in vitro and in vivo. |
Databáze: | OpenAIRE |
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