Aguilar-Villegas Óscar R, Barragán-Los Santos Javier, Del Moral-Wong Luis E, Amezcua-Guerra Luis M, Aguirre-García M Magdalena
Unidad de Investigación UNAM-INC, División de Investigación, Facultad de Medicina, Universidad Nacional Autónoma de México, Ciudad de México, México.
Departamento de Inmunología, Instituto Nacional de Cardiología Ignacio Chávez, Ciudad de México, México.
Arch Cardiol Mex. 2024 Oct 24;95(1):81-95. doi: 10.24875/ACM.23000246.
The formation of atherosclerotic plaque results from the complex interaction between modifiable and non-modifiable risk factors, through immune mechanisms that orchestrate both inflammatory and anti-inflammatory processes. Atherosclerosis often culminates in ischemic heart disease or cerebrovascular events, which are the leading causes of mortality worldwide. Currently, primary prevention focuses on controlling modifiable risk factors. Therefore, understanding the molecular mechanisms underlying the damage induced by these risk factors is essential to develop more effective treatments. This article provides a detailed review of the immunological processes underlying the initiation and progression of atheroma plaque, exploring their relationship with traditional risk factor such as smoking, diabetes mellitus, dyslipidemia, and hypertension, as well as a new potential risk factor: microbiota dysbiosis. Furthermore, the attributable risk of each factor is independently assessed, and the effectiveness of risk factor control measures is demonstrated as the best strategy to date for the regression of atherosclerosis and the prevention of its complications.
动脉粥样硬化斑块的形成源于可改变和不可改变的危险因素之间的复杂相互作用，通过协调炎症和抗炎过程的免疫机制实现。动脉粥样硬化常导致缺血性心脏病或脑血管事件，这是全球范围内的主要死亡原因。目前，一级预防侧重于控制可改变的危险因素。因此，了解这些危险因素所致损伤的分子机制对于开发更有效的治疗方法至关重要。本文详细综述了动脉粥样硬化斑块起始和进展的免疫过程，探讨了它们与吸烟、糖尿病、血脂异常和高血压等传统危险因素以及一种新的潜在危险因素：微生物群失调之间的关系。此外，还独立评估了每个因素的归因风险，并证明了危险因素控制措施的有效性是迄今为止使动脉粥样硬化消退和预防其并发症的最佳策略。
