NCS-1 knockout rendered mouse hearts more susceptible to oxidative/metabolic stress.
Re-expression of NCS-1 partially rescued cardiomyocytes from H2O2-induced toxicity
ATP levels, mitochondrial respiration and protein levels were lower in KO myocytes.
NCS-1 expression reversed early ΔΨm loss in KO myocytes induced by H2O2.
Stress-induced cardioprotective pathways were inhibited in KO hearts and myocytes.