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Statin therapy is known to potentiate the effect of antihypertensive drugs [32, 33] through vasodilation, which is due to increased nitric oxide synthase activity [34], downregulation of angiotensin II-type 1 receptors [35], and endothelin-1 production [36]

250 These mice exhibit impaired axonal mitochondrial membrane potential and bioenergetic function, indicating a lack of reserve capacity

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