Previous studies have shown that apoptosis via upregulation of pro-apoptotic Bax was induced in denervated muscle35 and that Ang II receptor blockade protected against apoptosis and atrophy in skeletal muscle of an experimental heart failure model36, which supports our results that deficiency in the AT1a receptor downregulated Bax gene expression and decreased the Bax/Bcl-2 ratio at 7 days postdenervation, and led to a lower number of TUNEL-positive nuclei at 21 days postdenervation. Here, BCL2 is linked to heart failure.