Inflammation
Lp(a) cardiovascular risk may run through inflammation, and lowering it partly reverses the inflammatory profile, a review (J Clin Lipidol 2023)
Original title: Lipoprotein(a) and inflammation- pathophysiological links and clinical implications for cardiovascular disease
This review examines the bidirectional relationship between Lp(a) and inflammation in cardiovascular disease. Lp(a), largely through oxidised phospholipids bound to its apolipoprotein(a) component, promotes monocyte activation and endothelial dysfunction, mechanisms supported mainly by experimental studies. Conversely, Lp(a) levels are themselves regulated by inflammatory stimuli and anti-inflammatory treatment. The authors note that reducing Lp(a) concentration, particularly with potent siRNA agents, partially reverses the Lp(a)-associated inflammatory profile, suggesting inflammation is both a consequence and a modifiable mediator of Lp(a)-driven cardiovascular risk.
Original abstract
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.
Summary written by lp-a.org from the published abstract; figures as published. Page updated 18 August 2026. Methods.