Key result
Prolonged cardiac calcium signaling drives maladaptive hypertrophy and heart failure despite physiological benefits.
This review highlights the complex, dual role of calcium signaling in both physiological cardiac function and the progression to pathological hypertrophy and heart failure.
Calcium modulation in hypertrophy warrants clinical caution; leaves open precise therapeutic targets pending prospective trials.
Ca(2+) increases in the heart control both contraction and transcription. To accommodate a short-term increased cardiovascular demand, neurohormonal modulators acting on the cardiac pacemaker and individual myocytes induce an increase in frequency and magnitude of myocyte contraction respectively. Prolonged, enhanced function results in hypertrophic growth of the heart, which is initially also associated with greater Ca(2+) signals and cardiac contraction. As a result of disease, however, hypertrophy progresses to a decompensated state and Ca(2+) signalling capacity and cardiac output are reduced. Here, the role that Ca(2+) plays in the induction of hypertrophy as well as the impact that cardiac hypertrophy and failure has on Ca(2+) fluxes will be discussed.
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Roderick et al. (2007) conducted a review in Cardiac hypertrophy and heart failure. Calcium signaling was evaluated. Calcium signaling plays a dual role in the heart, where physiological increases accommodate cardiovascular demand, but prolonged enhancement leads to maladaptive cardiac hypertrophy and heart failure.
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