Abstract
Renal failure, both acute and chronic, represents an important health problem by its social, sanitary and economic aspects. Mitogen-activated protein kinases (MAPK) are a family of mediators involved in the transduction of extracellular stimuli to intracellular responses. The best studied members of this family are extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), Jun NH2-terminal kinase (JNK), p38 kinase and extracellular signal regulated kinases 5 (ERK5) also known as big MAP Kinase 1 (BMK1). MAPKs plays a role in regulating renal function and all these pathways have been demonstrated to be activated in many “in vivo” and cellular models or renal failure. As MAP kinases are key regulators in the control of cell proliferation and cell death, many more or less specific inhibitors of these pathways are being developed for the treatment of tumors. The purpose of this review is to examine the data available on the role of MAPKs activation in “in vivo” models of renal failure, as well as in different renal cell types (especially in mesangial cells, podocytes, tubular epithelial cells and fibroblasts) subjected to stress or damage. We have also reviewed the effect of MAPKs inhibition on renal damage, both “in vivo” and “in vitro”. Data collected allow to suggest that therapy of chronic and acute renal disease with MAPKs inhibitors is a promising therapeutic area, although much more basic and clinical studies are necessary before this kind of therapy can be used in the everyday clinic.
Keywords: Acute renal failure, chronics renal failure, MAPkinase, ERK, JNK, p38kinase, fibroblasts, mesangial cells, podocytes, tubular epithelial cells
Current Medicinal Chemistry
Title: Therapeutical Relevance of MAP-Kinase Inhibitors in Renal Diseases: Current Knowledge and Future Clinical Perspectives
Volume: 15 Issue: 20
Author(s): M. Teresa Grande and Jose M. Lopez-Novoa
Affiliation:
Keywords: Acute renal failure, chronics renal failure, MAPkinase, ERK, JNK, p38kinase, fibroblasts, mesangial cells, podocytes, tubular epithelial cells
Abstract: Renal failure, both acute and chronic, represents an important health problem by its social, sanitary and economic aspects. Mitogen-activated protein kinases (MAPK) are a family of mediators involved in the transduction of extracellular stimuli to intracellular responses. The best studied members of this family are extracellular signal-regulated kinases 1 and 2 (ERK1 and ERK2), Jun NH2-terminal kinase (JNK), p38 kinase and extracellular signal regulated kinases 5 (ERK5) also known as big MAP Kinase 1 (BMK1). MAPKs plays a role in regulating renal function and all these pathways have been demonstrated to be activated in many “in vivo” and cellular models or renal failure. As MAP kinases are key regulators in the control of cell proliferation and cell death, many more or less specific inhibitors of these pathways are being developed for the treatment of tumors. The purpose of this review is to examine the data available on the role of MAPKs activation in “in vivo” models of renal failure, as well as in different renal cell types (especially in mesangial cells, podocytes, tubular epithelial cells and fibroblasts) subjected to stress or damage. We have also reviewed the effect of MAPKs inhibition on renal damage, both “in vivo” and “in vitro”. Data collected allow to suggest that therapy of chronic and acute renal disease with MAPKs inhibitors is a promising therapeutic area, although much more basic and clinical studies are necessary before this kind of therapy can be used in the everyday clinic.
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Cite this article as:
Grande Teresa M. and Lopez-Novoa M. Jose, Therapeutical Relevance of MAP-Kinase Inhibitors in Renal Diseases: Current Knowledge and Future Clinical Perspectives, Current Medicinal Chemistry 2008; 15 (20) . https://dx.doi.org/10.2174/092986708785132889
DOI https://dx.doi.org/10.2174/092986708785132889 |
Print ISSN 0929-8673 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-533X |
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