Researchers found that total left ventricular (LV) glutathione depletion in failing hearts was 54%, and that oral administration of the glutathione precursor N-acetylcysteine (NAC) inhibited neutral sphingomyelinase (N-SMase), Bcl-2 depletion, and caspase-3 activation, normalized LV glutathione, improved LV systolic function, and reduced adverse LV remodeling in rats after MI. Here, SMPD2 is linked to myocardial infarction.