Figure 10.

The proposed model for heart compensatory mechanism. (A) In normal, non-stressed conditions, HSR-related protein levels are reduced in old hearts and HSF1 is retained at the promoters of HSP genes. (B) Under stress conditions, HSF1 becomes hyperphosphorylated and actively promotes the transcription of HSP genes at a rate that is equivalent between young and old mice. Nevertheless, HSP accumulation is lower in old mice which could be a consequence of a slower rate of translation, an increased rate of degradation (perhaps due to a different tissue metabolism arising from compensatory remodelling of the heart) or sequestration of HSPs into amyloid deposits.