Specifically, the stability of the α1 isoform expression combined with low basal levels of endogenous CTS in the α1s/sα2s/s mice, in contrast to decreased NKA α1 expression levels and elevated CTS in disease models such as cardiac hypertrophy, heart failure, and cardiomyopathy [90,91,92,93,94,95] may explain the occurrence of physiological vs. pathological hypertrophy through the CTS/NKA receptor. Here, TTR is linked to heart failure.