Evidence from clinical and experimental studies has shown that HF increases systemic and myocardial oxidative stress.[36–38] By controlling redox pathway, BAs can protect the myocardium, both TCA and TCDCA have been shown to increase the expression of peroxisome proliferator-activated receptor gamma, Ras-related C3 botulinum toxin substrate 1, NADPH oxidase 4, p21CIP, and endothelial nitric oxide synthase.[39] Additionally, TGR5 overexpression reduced oxidative stress and inflammation by activating the AKT pathway in the cardiac myoblast cell line. This evidence concerns the gene GPBAR1 and hydrops fetalis.