Several epidemiological studies have clearly shown the high co-morbidity between depression and
Cardiovascular Diseases (CVD). Different studies have been conducted to identify the common pathophysiological events of these diseases such as the overactivation of the hypothalamic- pituitary-adrenal axis and, most importantly, the dysregulation of immune system which causes a chronic pro-inflammatory status. The biological link between depression,
inflammation, and CVD can be related to high levels of pro-inflammatory
cytokines, such as IL-1β, TNF-α, and
IL-6, released by macrophages which play a central role in the pathophysiology of both depression and CVD. Pro-inflammatory
cytokines interfere with many of the pathophysiological mechanisms relevant to depression by upregulating the rate-limiting
enzymes in the metabolic pathway of
tryptophan and altering
serotonin metabolism. These
cytokines also increase the risk to develop CVD, because activation of macrophages under this pro-inflammatory status is closely associated with endothelial dysfunction and oxidative stress, a preamble to
atherosclerosis and
atherothrombosis.
Carnosine (β-alanyl-
L-histidine) is an endogenous
dipeptide which exerts a strong antiinflammatory activity on macrophages by suppressing reactive species and pro-inflammatory
cytokines production and altering pro-inflammatory/anti-inflammatory macrophage polarization. This
dipeptide exhibits
antioxidant properties scavenging reactive species and preventing oxidative stress-induced pathologies such as CVD. In the present review we will discuss the role of oxidative stress and chronic
inflammation as common pathophysiological events both in depression and CVD and the preclinical and clinical evidence on the protective effect of
carnosine in both diseases as well as the therapeutic potential of this
dipeptide in depressed patients with a high co-morbidity of
cardiovascular diseases.