Psoriasis and Cardiometabolic Diseases: Shared Genetic and Molecular Pathways

Abstract

A convincing deal of evidence supports the fact that severe psoriasis is associated with cardiovascular diseases. However, the precise underlying mechanisms linking psoriasis and cardiovascular diseases are not well defined. Psoriasis shares common pathophysiologic mechanisms with atherosclerosis and cardiovascular (CV) risk factors. In particular, polymorphism in the IL-23R and IL-23 genes, as well as other genes involved in lipid and fatty-acid metabolism, renin-angiotensin system and endothelial function, have been described in patients with psoriasis and with cardiovascular risk factors. Moreover, systemic inflammation in patients with psoriasis, including elevated serum proinflammatory cytokines (e.g., TNF-α, IL-17, and IL-23) may contribute to an increased risk of atherosclerosis, hypertension, alteration of serum lipid composition, and insulin resistance. The nonlinear and intricate interplay among various factors, impacting the molecular pathways in different cell types, probably contributes to the development of psoriasis and cardiovascular disease (CVD). Future research should, therefore, aim to fully unravel shared and differential molecular pathways underpinning the association between psoriasis and CVD.

Keywords: MACE; atherosclerosis; cardiovascular; diabetes; hyperlipidemia; hypertension; myocardial infarction; obesity; psoriasis.

Figure 1

Molecular pathways involved in the link between psoriasis and its comorbidities. Psoriasis per se is considered an independent risk factor for atherosclerosis. Moreover, psoriasis is also associated with a high prevalence of traditional modifiable CV risk factors, such as hypertension, diabetes, hyperlipidemia, obesity, and nonalcoholic fatty liver disease (NAFLD) [27,28,29]. Aberrantly activated molecular pathways involved in the link between psoriasis and its comorbidities are indicated.