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Am J Physiol Renal Physiol 279: F593-F604, 2000;
0363-6127/00 $5.00
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Vol. 279, Issue 4, F593-F604, October 2000

INVITED REVIEW
MAPK signaling and the kidney

Wei Tian, Zheng Zhang, and David M. Cohen

Divisions of Nephrology and Molecular Medicine, Oregon Health Sciences University, and Portland Veterans Affairs Medical Center, Portland, Oregon 97201

Following an overview of the biochemistry of mitogen-activated protein kinase (MAPK) pathways, the relevance of these signaling events to specific models of renal cell function and pathophysiology, both in vitro and in vivo, will be emphasized. In in vitro model systems, events activating the principal MAPK families [extracellular signal-regulated and c-Jun NH2-terminal kinase and p38] have been best characterized in mesangial and tubular epithelial cell culture systems and include peptide mitogens, cytokines, lipid mediators, and physical stressors. Several in vivo models of proliferative or toxic renal injury are also associated with aberrant MAPK regulation. It is anticipated that elucidation of downstream effector signaling mechanisms and a clearer understanding of the immediate and remote upstream activating pathways, when applied to these highly clinically relevant model systems, will ultimately provide much greater insight into the basis for specificity now seemingly absent from these signaling events.

urea; tubule; mesangial; extracellular signal-regulated kinase; stress-activated protein kinase; c-Jun NH2-terminal kinase; p38; mitogen-activated protein kinase


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