Signalling pathways in pressure-overload cardiac hypertrophy

Cardiac hypertrophy, i.e., enlargement of cardiomyocytes (adult cardiomyocytes are terminally differentiated and nonproliferative), may be caused by a variety of physiological and pathogenic stimuli such as pressure or volume overload. However, cardiac hypertrophy is not only an adaptational state to, e.g., high blood pressure or heart valve stenosis, before heart failure occurs but per se is a risk factor for severe cardiac events such as arrhythmia, ischemia, and sudden death. Different signalling pathways of cardiac hypertrophy activated, for example, by mechanical stress, hypoxia and neurohumoral stimuli, are complex and have only been partly elucidated. So far, several intra-cellular signalling components have been associated with the induction of cardiac hypertrophy, including G-proteins, phospholipases, protein kinases, protein phosphatases, and several transcription factors, finally leading to the cellular enlargement. The present short review of the extracellular stimuli and signalling pathways involved in the generation of pressure-overload hypertrophy are summarized. A comprehensive elucidation of its pathogenesis may lead to a therapeutic intervention in the future.