Figure 1.

Here we propose an alternative “heatsensing” model in which exposure to heat or treatment with capsaicin resulted in HSR activation, through TRPV1, by yet unknown interim cellular mediators (1) Capsazepine, a selective antagonist of TRPV1, abolishes the heat- or capsaicin-induced activation of the HSR and the consequent accumulation of Hsp70, 90, and 25 chaperones. This model is an alternative to the current prevailing proposed mechanism suggesting that under stress, misfolded proteins recruit HSF1-interacting Hsps thereby allowing HSF1 activation (2).