Role of the JAK/STAT signaling pathway in diabetic nephropathy
| Autor: | David M. Stern, Amy K.L. Banes-Berceli, Mario B. Marrero, Douglas C. Eaton |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
medicine.medical_specialty
Mesangial cell Physiology Chemistry Renal glomerulus Angiotensin II Glomerular Mesangial Cell Kidney Glomerulus JAK-STAT signaling pathway Protein-Tyrosine Kinases medicine.disease Diabetic nephropathy STAT Transcription Factors Glucose Polyol pathway Endocrinology Internal medicine medicine Cancer research Humans Diabetic Nephropathies Janus kinase Signal Transduction |
| Zdroj: | American Journal of Physiology-Renal Physiology. 290:F762-F768 |
| ISSN: | 1522-1466 1931-857X |
| DOI: | 10.1152/ajprenal.00181.2005 |
| Popis: | Excessive cellular growth is a major contributor to pathological changes associated with diabetic nephropathy. In particular, high glucose-induced growth of glomerular mesangial cells is a characteristic feature of diabetes-induced renal complications. Glomerular mesangial cells respond to traditional growth factors, although in diabetes this occurs in the context of an environment enriched in both circulating vasoactive mediators and high glucose. For example, the vasoactive peptide ANG II has been implicated in the pathogenesis of diabetic renal disease, and recent findings suggest that high glucose and ANG II activate intracellular signaling processes, including the polyol pathway and generation of reactive oxygen species. These pathways activate the Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling cascades in glomerular mesangial cells. Activation of the JAK/STAT signaling cascade can stimulate excessive proliferation and growth of glomerular mesangial cells, contributing to diabetic nephropathy. This review focuses on some of the key elements in the diabetic microenvironment, especially high glucose and the accumulation of advanced glycoxidation end products and considers their impact on ANG II and other vasoactive peptide-mediated signaling events in vitro and in vivo. |
| Databáze: | OpenAIRE |
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