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Understanding the cellular signals that initiate cardiac hypertrophy is of critical importance in identifying the pathways that mediate heart failure. The family of mitogen-activated protein kinases (MAPKs), including the extracellular signal-regulated kinases (ERKs), c-Jun NH(2)-terminal kinase (JNK), and p38 MAPKs, may play specific roles in myocardial growth and function.

circulation

Cardiac Overexpression of a G <sub>q</sub> Inhibitor Blocks Induction of Extracellular Signal–Regulated Kinase and c-Jun NH <sub>2</sub> -Terminal Kinase Activity in In Vivo Pressure Overload

Cardiac Overexpression of a G q Inhibitor Blocks Induction of Extracellular Signal–Regulated Kinase and c-Jun NH 2 -Terminal Kinase Activity in In Vivo Pressure Overload

Cardiac Overexpression of a G _q Inhibitor Blocks Induction of Extracellular Signal–Regulated Kinase and c-Jun NH ₂ -Terminal Kinase Activity in In Vivo Pressure Overload