MAPK signaling and the kidney

Wei Tian, Zheng Zhang, David M. Cohen

Research output: Contribution to journalReview article

142 Scopus citations

Abstract

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.

Original languageEnglish (US)
Pages (from-to)F593-F604
JournalAmerican Journal of Physiology - Renal Physiology
Volume279
Issue number4 48-4
DOIs
StatePublished - 2000

Keywords

  • Extracellular signal-regulated kinase
  • Mesangial
  • Mitogen-activated protein kinase
  • Stress-activated protein kinase
  • Tubule
  • Urea
  • c-Jun NH-terminal kinase
  • p38

ASJC Scopus subject areas

  • Physiology
  • Urology

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