Reconciling depressed Ca2+ sparks occurrence with enhanced RyR2 activity in failing mice cardiomyocytes

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Ruiz-Hurtado, Gema | Li, Linwei | Fernández-Velasco, María | Rueda, Angélica | Lefebvre, Florence | Wang, Yueyi | Mateo, Philippe | Cassan, Cécile | Gellen, Barnabas | Benitah, Jean, Pierre | Gómez, Ana, María

Edité par CCSD ; Rockefeller University Press -

International audience. Cardiovascular disease is the leading cause of death in the world (Dahlöf, 2010; Lloyd-Jones, 2010). Heart failure (HF) supports an important percentage of the cardiovascular diseases with serious clinical complications including cardiac arrhythmias, in many cases derived from calcium (Ca 2+)-handling impairment. Among others, Ca 2+ is a key factor of electrical activation, ion channel gating, and excitation-contraction (EC) coupling in the cardiac muscle. During cardiac EC coupling, Ca 2+ influx via sarcolemmal L-type Ca 2+ channels triggers Ca 2+

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