Cellular stress responses and molecular mechanisms of nephrotoxicity

Toxicol Lett. 2006 Mar 15;162(1):83-93. doi: 10.1016/j.toxlet.2005.10.014. Epub 2005 Dec 15.

Abstract

Increasing our knowledge on the molecular and cellular mechanisms of acute renal tubular pathologies will lead to potential novel therapeutic strategies either to prevent the initiation of renal failure or to promote the renal regeneration after injury. Currently many genomic- and proteomic-based techniques are available to identify genes, proteins or protein modifications in relation to renal toxicity. Although we are able to identify many genes and proteins at once, the actual role of the genes and proteins with respect to cellular toxicity needs to be defined in order to better understand the molecular basis of renal cell injury and repair. This review will focus on the relationship between changes in gene and protein expression, cellular perturbations, signal transduction, and mechanisms of toxicity. A focus is on the role of stress response proteins in repair of injured renal cells.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Apoptosis
  • Endoplasmic Reticulum / metabolism
  • Gene Expression Regulation
  • HSP70 Heat-Shock Proteins / metabolism
  • Heat-Shock Proteins / metabolism
  • Humans
  • Kidney Diseases / genetics
  • Kidney Diseases / metabolism*
  • Membrane Proteins / metabolism
  • Protein Kinases / metabolism
  • Proto-Oncogene Proteins c-myc / metabolism
  • Signal Transduction
  • Toxicogenetics*
  • Transcription Factor CHOP / metabolism

Substances

  • HSP70 Heat-Shock Proteins
  • Heat-Shock Proteins
  • Membrane Proteins
  • Proto-Oncogene Proteins c-myc
  • glucose-regulated proteins
  • Transcription Factor CHOP
  • Protein Kinases