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

Gema Ruiz-Hurtado (1) , Linwei Li (1) , María Fernández-Velasco (2) , Angélica Rueda (3) , Florence Lefebvre (1) , Yueyi Wang (1) , Philippe Mateo (1) , Cécile Cassan (4) , Barnabas Gellen (5) , Jean Pierre Benitah (1) , Ana María Gómez (1)

1 Signalisation et physiopathologie cardiaque
2 IdiPAZ - Instituto de Investigacion Hospital La Paz
3 Physiopathologie cardiovasculaire
4 MIVEGEC - Maladies infectieuses et vecteurs : écologie, génétique, évolution et contrôle
5 CHU Henri Mondor - Département de physiologie

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+

Mots clés: EC; excitation-contraction; FDHM; full duration at half-maximum; FWHM; full width at half-maximum; HF; heart failure; NCX; sodium-calcium exchanger; PLB; phospholamban; PMI; post-myocardial infarction; SERCA; sarco-endoplasmic reticulum Ca 2+ ATPase

Domaines: Sciences du Vivant [q-bio]

Gema Ruiz-Hurtado, Linwei Li, María Fernández-Velasco, Angélica Rueda, Florence Lefebvre, et al.. Reconciling depressed Ca2+ sparks occurrence with enhanced RyR2 activity in failing mice cardiomyocytes. Journal of General Physiology, 2015, 146 (4), pp.295-306. ⟨10.1085/jgp.201511366⟩. ⟨hal-03095795⟩