Fig. 9

Schematic diagram showing the protective effect of Ang-(1–7) on SIC mice and its underlying mechanism. LPS can induce RAAS activation and increase Ang II secretion in blood, tissues, and cells. LPS and Ang II can activate NF-κB and MAPK pathways and generate a large number of inflammatory mediators. Excessive production of proinflammatory factors aggravates oxidative stress, mitochondrial damage, and dynamic imbalance in cardiomyocytes, and further leads to increased apoptosis of cardiomyocytes. Ang-(1–7) may regulate inflammation, reduce oxidative stress, maintain mitochondrial homeostasis, and alleviate mitochondrial structural and functional damage through NF-κB and MAPK pathways