Similarly, in a study on the relationship between mitochondrial respiration and fatal aortic dissection in patients and in angiotensin II-induced aortic aneurysms in ApoE knockout mice, the mitochondrial respiration-related proteins and the cell oxygen consumption rate are reduced, but the production of lactate is increased, while nicotinamide riboside treatment can reduce the development of aortic aneurysms and sudden death caused by aortic aneurysm rupture in mice [5]. The gene discussed is APOE; the disease is aortic aneurysm.