Fig. 5
This scheme illustrates the proposed role of AC5 in the heart of PG-LPS-treated mice. Mice with experimental periodontitis induced by the ligation of the left first molar [39] or by chronic PG-LPS infusion as used in this study [18] show sympathetic overactivity. β-AR/GSα/AC5 signaling is activated by PG-LPS treatment, leading to ROS production via NOX4 and PLN phosphorylation at Thr-17. These changes might cause fibrosis and myocyte apoptosis in the heart of PG-LPS-treated mice, leading to cardiac dysfunction