Abstract
Ca2+ entry through L-type Ca2+ channels (LTCCs) is crucial for cardiac excitability and contraction. During the fight-or-flight response, β-adrenergic stimulation of LTCC currents contributes to the increase of the cardiac contractility. Nevertheless, long-term stimulation alters Ca2+ cycling, leading to heart failure. To date, the contribution of LTCC to heart failure remains speculative. Modifying auxiliary subunits in transgenic mouse models altered LTCC currents but the role of LTCC currents in heart failure remains unconclusive. This review recapitulates a vast and evolving literature on the protein interaction within the LTCC complex, its impact on LTCC-mediated-Ca2+ signaling, and cardiac hypertrophy and heart failure.
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