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Additionally, BBR may regulate the mTOR pathway to suppress the phosphorylation of ERK1/2 and p38, increase autophagy, alleviate ER stress, and activate the Pak1 pathway to inhibit Fbxo32 upregulation, lower myocardial cell Ca 2+ concentration, reduce left ventricular end-diastolic pressure, upregulate PINK1/Parkin-mediated mitochondrial autophagy, and thus inhibit myocardial cell apoptosis and mitochondrial damage, improving heart failure and myocardial hypertrophy ( 7.2.6 Thrombosis BBR reduces thrombus formation by inhibiting CutC enzyme activity and decreasing TMAO production (Qu et al., 2024)
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