Lipoprotein(a) and inflammation-pathophysiological links and clinical implications for cardiovascular disease

The role of lipoprotein(a) (Lp[a]) as a significant and possibly causal cardiovascular disease (CVD) risk factor has been well established. Many studies, mostly experimental, have supported inflammation as a mediator of Lp(a)-induced increase in CVD risk. Lp(a), mainly through oxidized phospholipids bound to its apolipoprotein(a) part, leads to monocyte activation and endothelial dysfunction. The relationship between Lp(a) and inflammation is bidirectional as Lp(a) levels, besides being associated with inflammatory properties, are regulated by inflammatory stimuli or anti-inflammatory treatment. Reduction of Lp(a) concentration, especially by potent siRNA agents, contributes to partial reversion of the Lp(a) related inflammatory profile. This review aims to present the current pathophysiological and clinical evidence of the relationship between Lp(a) and inflammation. (c) 2022 National Lipid Association. Published by Elsevier Inc. All rights reserved.

Automated summary

The role of lipoprotein(a) (Lp[a]) as a significant and possibly causal cardiovascular disease (CVD) risk factor has been well established. Many studies have supported inflammation as a mediator of Lp(a)-induced increase in CVD risk. The relationship between Lp(a) and inflammation is bidirectional as Lp(a) levels are regulated by inflammatory stimuli or anti-inflammatory treatment, and reduction of Lp(a) concentration contributes to partial reversion of the Lp(a) related inflammatory profile.