Simantiris Spyridon, Antonopoulos Alexios S, Papastamos Charalampos, Benetos Georgios, Koumallos Nikolaos, Tsioufis Konstantinos, Tousoulis Dimitris
1st Cardiology Department, Hippokration Hospital, National and Kapodistrian University of Athens, Vas. Sofias Avenue 114, Athens 11527, Greece (Drs Simantiris, Antonopoulos, Papastamos, Benetos, Tsioufis, and Tousoulis).
Department of Cardiothoracic Surgery, Hippokration Hospital, Athens, Greece (Dr Koumallos).
J Clin Lipidol. 2023 Jan-Feb;17(1):55-63. doi: 10.1016/j.jacl.2022.10.004. Epub 2022 Oct 20.
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.
脂蛋白(a) [Lp(a)]作为一种重要且可能是导致心血管疾病(CVD)的危险因素，其作用已得到充分证实。许多研究（大多为实验性研究）支持炎症是Lp(a)导致CVD风险增加的介导因素。Lp(a)主要通过与其载脂蛋白(a)部分结合的氧化磷脂，导致单核细胞活化和内皮功能障碍。Lp(a)与炎症之间的关系是双向的，因为Lp(a)水平除了与炎症特性相关外，还受炎症刺激或抗炎治疗的调节。降低Lp(a)浓度，尤其是通过有效的小干扰RNA (siRNA)制剂降低Lp(a)浓度，有助于部分逆转与Lp(a)相关的炎症特征。本综述旨在介绍Lp(a)与炎症之间关系的当前病理生理学和临床证据。
