All organisms exposed to environmental stress conditions share a commo
n molecular response characterized by a dramatic change in the pattern
of gene expression followed by an elevated synthesis of heat shock or
stress proteins. These proteins function as molecular chaperones to p
rotect cells from environmental stress damage by binding to partially
denatured proteins, dissociating protein aggregates, and regulating th
e correct folding and intracellular translocation of newly synthesized
polypeptides. Accumulating evidence supports a role for heat shock pr
oteins in a number of disease states of which inflammatory reactions a
nd ischaema provide the best studied examples. The inducible heat shoc
k response involves transcriptional gene activation mediated by specif
ic regulatory proteins called heat shock transcription factors, which
bind to the promoter of heat shock genes in a sequence-specific manner
, However, the signalling pathways leading to the activation of these
transcription factors need to be characterized in more detail to be ab
le to understand the role, cause, or consequence, of heat shock protei
ns in human diseases, This review presents recent progress in unravell
ing the regulation of heat shock gene expression in cells subjected to
heat or other forms of stress, By using inflammatory responses and my
ocardial ischaema as examples, the putative use of heat shock proteins
are discussed as targets for future therapeutic applications.