Hsp60 chaperonopathies and chaperonotherapy: targets and agents

The information available encourages the development of ways to improve Hsp60 activity (positive chaperonotherapy) when deficient or to block it (negative chaperonotherapy) when pathogenic. Many questions are still unanswered and obstacles are obvious. More information is needed to establish when and why autologous Hsp60 becomes a pathogenic autoantigen, or induces cytokine formation and inflammation, or favors carcinogenesis. Clarification of these points will take considerable time. However, analysis of the Hsp60 molecule and a search for active compounds aimed at structural sites that will affect its functioning should continue without interruption. No doubt that some of these compounds will offer therapeutic hopes and will also be instrumental for dissecting structure-function relationships at the biochemical and biological (using animal models and cultured cells) levels.