Key result
Targeting Ca(2+) channel-blocking Rem proteins to caveolin-3-containing membranes eliminated Ca(2+) influx-induced NFAT nuclear translocation without reducing myocyte contractility.
Population
Cardiac myocytes (preclinical model)
Design
Preclinical
Authors
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May enable hypertrophy suppression without contractile impairment; hypothesis-generating in animal models and leaves open human translation.
Targeting L-type calcium channels specifically within caveolae signaling domains can inhibit pathological hypertrophic signaling without impairing cardiac contractility.
Makarewich et al. (2012) studied Pathological cardiac hypertrophy. Ca(2+) channel-blocking Rem proteins targeted to Cav-3-containing membranes was evaluated on NFAT nuclear translocation and myocyte contractility. Targeting Ca(2+) channel-blocking Rem proteins to caveolin-3-containing membranes eliminated Ca(2+) influx-induced NFAT nuclear translocation without reducing myocyte contractility.
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