Posadas-Sánchez Rosalinda, Vargas-Alarcón Gilberto
Department of Endocrinology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Department of Molecular Biology, Instituto Nacional de Cardiología Ignacio Chávez, Mexico City, Mexico.
Rev Invest Clin. 2018;70(1):5-17. doi: 10.24875/RIC.17002335.
Atherosclerosis is a chronic, progressive, and multifactorial disease modulated by genetic and environmental factors. In recent years, the paradigm that explained atherosclerosis as resulting from a complex interaction between factors not accessible to medical intervention, and modifiable risk factors has changed. In this paradigm, alterations in lipid metabolism were the pivotal concept of atherosclerosis as a chronic degenerative disease. In the last years, an increasing number of observations have shown that the innate and adaptive immune responses to lipoprotein deposition and oxidation in the arterial wall significantly influence atherosclerosis. Currently, it is well recognized that the pathogenesis of atherosclerosis and its complications involves the inflammatory process, which includes the participation of several cytokines. Besides the classic cytokines involved in this process, the role of the interleukin-12 (IL-12) family has been recently demonstrated. This review describes our current understanding about the role of the family of IL-12 in atherosclerosis considering the participation of the genes that encode these cytokines in the genetic susceptibility to developing this disease.
动脉粥样硬化是一种由遗传和环境因素调节的慢性、进行性和多因素疾病。近年来，将动脉粥样硬化解释为由医学干预无法触及的因素与可改变的危险因素之间复杂相互作用导致的范式已经改变。在这种范式中，脂质代谢改变是动脉粥样硬化作为一种慢性退行性疾病的关键概念。在过去几年中，越来越多的观察结果表明，对动脉壁中脂蛋白沉积和氧化的先天性和适应性免疫反应会显著影响动脉粥样硬化。目前，人们已经充分认识到动脉粥样硬化及其并发症的发病机制涉及炎症过程，其中包括多种细胞因子的参与。除了参与这一过程的经典细胞因子外，白细胞介素-12（IL-12）家族的作用最近也得到了证实。本综述考虑了编码这些细胞因子的基因在患此病的遗传易感性中的参与情况，描述了我们目前对IL-12家族在动脉粥样硬化中作用的理解。
