Cardiovascular disease, the foremost cause of death worldwide, is an overarching disease term that encompasses a number of disorders involving the heart and circulatory system, including atherosclerosis. Atherosclerosis is a primary cause of cardiovascular diseases and is caused by buildup of plaque and narrowing of blood vessels. Epidemiological studies have suggested that environmental pollutants are implicated in atherosclerosis disease progression. Among many environmental pollutants, acrolein (Acr) is an abundant reactive aldehyde and is ubiquitously present in cigarette smoke as well as food products (e.g., overheated oils and wine). Despite its ubiquitous presence and potential impact on the etiology of cardiovascular disease, a limited consensus has been made in regard to Acr exposure conditions to induce atherosclerosis in vivo. This mini-review summarizes in vivo atherosclerosis models using Acr to investigate biochemical and phenotypic changes related to atherosclerosis and in vitro mechanistic studies involving Acr and atherosclerosis.

心血管疾病是全世界最主要的死亡原因，是一个包罗万象的疾病术语，涵盖了许多涉及心脏和循环系统的疾病，包括动脉粥样硬化。动脉粥样硬化是心血管疾病的主要原因，是由斑块积聚和血管狭窄引起的。流行病学研究表明环境污染物与动脉粥样硬化疾病的进展有关。在众多环境污染物中，丙烯醛（Acr）是一种含量丰富的活性醛，普遍存在于香烟烟雾以及食品（例如过热的油和酒）中。尽管 Acr 普遍存在并且对心血管疾病的病因学具有潜在影响，但关于 Acr 暴露条件在体内诱导动脉粥样硬化的问题尚未达成有限的共识。这篇小综述总结了使用 Acr 的体内动脉粥样硬化模型来研究与动脉粥样硬化相关的生化和表型变化，以及涉及 Acr 和动脉粥样硬化的体外机制研究。