C3-fed mice had reduced cardiac hypertrophy, fibrosis, vascular dysfunction, and hypertension in the hypertensive model compared to control mice, which also reduced susceptibility to arrhythmias and atherosclerosis lesions.39 In addition, C3 affects the release of renin and the level of Ang II in plasma through the kidney olfr78 receptor.36 In this study, we show that C3 inhibits the rapid increase of Ang II levels during reperfusion and reduces myocardial I/R injury through GPR41. This evidence concerns the gene FFAR3 and cardiac hypertrophy.