Atherosclerosis, a disease characterized by the accumulation of lipid-rich plaques in medium to large arteries, represents the most common cause of death in the world. Mitochondrial dysfunction contributes to many steps of the disease, through the production of reactive oxygen species (ROS) and by disrupting cell signalling pathways. Importantly, ROS induce the dedifferentiation of vascular smooth muscle cells, after which they migrate to the plaque region and proliferate, rendering the disease irreversible. The western diet (W-DIET), rich in unhealthy fats and sugars, contributes to the epidemic of obesity and metabolic diseases, leading many individuals to alternative dietary patterns, including the low-carbohydrate high-protein diet (L-DIET). However, emerging evidence, both in humans and in animals, show that the L-DIET could worsen the progression of atherosclerosis, although the pathways through which the plaque buildup occurs remains largely unknown. In parallel, poor dietary patterns induce gut dysbiosis, which represents a major driver of diseases and strongly correlates with the development of cardiovascular pathologies. Hence, by restoring the integrity of the gut microbiota, probiotics supplements could prevent the buildup of atherosclerotic plaques. Using a meta-analysis, high-resolution respirometry, immunoblotting, and polymerase chain reaction sequencing, this thesis explores the role of (1) supplements of probiotics and (2) the L-DIET in modulating oxidative stress, the mitochondria, and the gut bacterial composition. The data reported here present evidence that the L-DIET could induce mitochondrial dysfunction and gut-dysbiosis. The results also support that by improving mitochondrial integrity and biomarkers of oxidative stress, probiotics represent an affordable, low-risk alternative treatment in the prevention of atherosclerosis.