Molecular interplay between mechanical and humoral signalling in cardiac hypertrophy.

Heart failure is a major clinical problem, only partly mitigated by current pharmacological therapy. An early marker of heart failure is hypertrophic remodelling of the heart, which represents a compensatory mechanism for the mechanical stress imposed by haemodynamic overload, but can eventually affect cardiac function. Recently, using genetically modified animals, have we started to identify the molecular components that elaborate the mechanical stimulus leading to cardiac hypertrophy, with its beneficial and detrimental effects. Characterization of the relative roles of the molecules implicated in the signalling pathways involved in the hypertrophic process might allow us to control the hypertrophic response to haemodynamic overload, directing it to more favourable outcomes.