MTOR and hypertrophy: Studies have shown that by inhibiting the activity of the mammalian target of rapamycin (mTOR) and the phosphorylation of its upstream extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein kinase (MAPK), BBR (10 mg/kg/d, p.o., 4 weeks) could enhance autophagy and inhibit ER stress, thus playing an important role in preventing pressure overload-induced myocardial hypertrophy and apoptosis (Li et al., 2014; Hashemzaei et al., 2017; Chen et al., 2020).