<oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd">
  <dc:creator>Lovis C</dc:creator>
  <dc:creator>Mach F</dc:creator>
  <dc:creator>Donati YR</dc:creator>
  <dc:creator>Bonventre JV</dc:creator>
  <dc:creator>Polla BS</dc:creator>
  <dc:date>1994</dc:date>
  <dc:description xmlns:ns0="xml" ns0:lang="en">The heat shock (HS) response is remarkably conserved during evolution and is evoked under many conditions of stress. There are a number of ways in which this ubiquitous response may be important for the understanding of renal pathophysiology. Ischemia, toxin exposure, and oxidative stress induce this response. Several models of hypertension are associated with increased susceptibility to environmental stress and increased accumulation of heat shock protein mRNA. HSP70 polymorphism has been demonstrated when comparing normotensive and hypertensive rats. Heat shock proteins may play a role in renal diseases through their important involvement in immunological processes. Several observations point to a role of the heat shock response in systemic lupus erythematosus (SLE). Autoantibodies against HSP70 and ubiquitin are found in many patients with this disease. Autoantibodies against ubiquitin and ubiquitinated histone H2A are localized to the kidney glomerular basement membrane of SLE patients with active disease. A better understanding of the HS response may thus provide important insight into renal pathophysiology and may suggest paradigms for therapeutic interventions.</dc:description>
  <dc:identifier>https://sonar.ch/global/documents/10612</dc:identifier>
  <dc:language>eng</dc:language>
  <dc:relation>info:eu-repo/semantics/altIdentifier/doi/10.3109/08860229409044859</dc:relation>
  <dc:relation>info:eu-repo/semantics/altIdentifier/pmid/8041958</dc:relation>
  <dc:source>Renal failure. - 1994</dc:source>
  <dc:subject xmlns:ns1="xml" ns1:lang="en">Adult</dc:subject>
  <dc:subject xmlns:ns2="xml" ns2:lang="en">Autoantigens</dc:subject>
  <dc:subject xmlns:ns3="xml" ns3:lang="en">Autoimmunity</dc:subject>
  <dc:subject xmlns:ns4="xml" ns4:lang="en">Drug Resistance</dc:subject>
  <dc:subject xmlns:ns5="xml" ns5:lang="en">Female</dc:subject>
  <dc:subject xmlns:ns6="xml" ns6:lang="en">Heat-Shock Proteins</dc:subject>
  <dc:subject xmlns:ns7="xml" ns7:lang="en">Humans</dc:subject>
  <dc:subject xmlns:ns8="xml" ns8:lang="en">Hypertension</dc:subject>
  <dc:subject xmlns:ns9="xml" ns9:lang="en">Kidney</dc:subject>
  <dc:subject xmlns:ns10="xml" ns10:lang="en">Lupus Erythematosus, Systemic</dc:subject>
  <dc:subject xmlns:ns11="xml" ns11:lang="en">Male</dc:subject>
  <dc:subject xmlns:ns12="xml" ns12:lang="en">Middle Aged</dc:subject>
  <dc:subject xmlns:ns13="xml" ns13:lang="en">Polymorphism, Genetic</dc:subject>
  <dc:subject xmlns:ns14="xml" ns14:lang="en">Reperfusion Injury</dc:subject>
  <dc:title xmlns:ns15="xml" ns15:lang="en">Heat shock proteins and the kidney.</dc:title>
  <dc:type>http://purl.org/coar/resource_type/c_6501</dc:type>
</oai_dc:dc>
