Fig. 7. Schematic representation of the proposed mechanism, based on our current and previous findings. Under control conditions (A), myocardial stretch triggers p38-MAPK activation and DUSP6 up-regulation, therefore restricting the increase in ERK1/2-p90RSK and NHE-1 phosphorylation/activation [14, 25], with the consequent limitation of the SFR amplitude. Prevention of p38-MAPK activation (B) precludes DUSP6 up-regulation after stretch allowing a higher phosphorylation of ERK1/2-p90RSK and consequently of NHE-1, leading to a greater increase in force during the SFR development.