Endothelial dysfunction involving dysfunctional mitochondria precedes the development of cardiovascular diseases.
This impairment results from an increase in reactive oxygen species, which leads to oxidative stress and a reduced
bioavailability of nitric oxide. It has been demonstrated that oxidative stress and alterations in glucose and lipid homeostasis
(e.g. hyperinsulinemia, hyperglycemia, insulin resistance and dyslipidemia) are linked to mitochondrial impairment
and that all of them contribute to endothelial dysfunction. Anti-hyperlipidemic drugs such as statins, anti-hypertensive
drugs and angiotensin receptor antagonists have been shown to exert protection through anti-oxidative stress mechanisms.
Other substances with antioxidant properties, such as vitamins, are also capable of abolishing the oxidative stress associated
with cardiometabolic diseases. However, the results obtained with general antioxidants in clinical trials are contradictory,
perhaps due to the unspecific nature of the targets selected. This study correlates endothelial dysfunction and mitochondrial
dysfunction and examines current research for the selective targeting of specific molecules (such as ·NO donors
and antioxidants) to mitochondria with the aim of protecting the endothelium against oxidative stress in cardiovascular