心血管疾病(CVD)的全球患病率继续稳步上升,使其成为全球死亡的主要原因。动脉粥样硬化(AS)是这些疾病的主要驱动因素,在幼年时期默默地开始,并最终导致严重影响患者生活质量或导致死亡的不良心血管事件。血脂异常,尤其是低密度脂蛋白胆固醇(LDL-C)水平升高,作为独立的危险因素,在AS发病机制中起着举足轻重的作用。研究表明,动脉壁内异常的LDL-C积累是动脉粥样硬化斑块形成的关键触发因素。随着疾病的进展,斑块积聚可能会破裂或移位,导致血栓形成和完全的血液供应阻塞,最终导致心肌梗塞,脑梗塞,和其他常见的不良心血管事件。尽管有足够的药物治疗以降低LDL-C为目标,有心脏代谢异常的患者仍有很高的疾病复发风险,强调解决LDL-C以外的脂质风险因素的重要性最近的注意力集中在甘油三酯之间的因果关系上,富含甘油三酯的脂蛋白(TRLs),以及他们在AS风险中的残余物。遗传,流行病学,临床研究表明,TRLs及其残留物与AS风险增加之间存在因果关系,这种血脂异常可能是不良心血管事件的独立危险因素。特别是在肥胖患者中,代谢综合征,糖尿病,和慢性肾病,TRLs紊乱及其残余水平显著增加动脉粥样硬化和心血管疾病发展的风险.过度合成的TRLs在血浆中的积累,TRLs脂解酶功能受损,和受损的肝脏清除富含胆固醇的TRLs残余物可导致TRLs及其残余物的动脉沉积,促进泡沫细胞形成和动脉壁炎症。因此,了解TRLs诱导的AS的发病机制和靶向治疗可以减缓或阻碍AS的进展,从而降低心血管疾病的发病率和死亡率,尤其是冠状动脉粥样硬化性心脏病。
The global prevalence of cardiovascular diseases (CVD) continues to rise steadily, making it a leading cause of mortality worldwide. Atherosclerosis (AS) serves as a primary driver of these conditions, commencing silently at an early age and culminating in adverse cardiovascular events that severely impact patients\' quality of life or lead to fatality. Dyslipidemia, particularly elevated levels of low-density lipoprotein cholesterol (LDL-C), plays a pivotal role in AS pathogenesis as an independent risk factor. Research indicates that abnormal LDL-C accumulation within arterial walls acts as a crucial trigger for atherosclerotic plaque formation. As the disease progresses, plaque accumulation may rupture or dislodge, resulting in thrombus formation and complete blood supply obstruction, ultimately causing myocardial infarction, cerebral infarction, and other common adverse cardiovascular events. Despite adequate pharmacologic therapy targeting LDL-C reduction, patients with cardiometabolic abnormalities remain at high risk for disease recurrence, highlighting the importance of addressing lipid risk factors beyond LDL-C. Recent attention has focused on the causal relationship between triglycerides, triglyceride-rich lipoproteins (TRLs), and their remnants in AS risk. Genetic, epidemiologic, and clinical studies suggest a causal relationship between TRLs and their remnants and the increased risk of AS, and this dyslipidemia may be an independent risk factor for adverse cardiovascular events. Particularly in patients with obesity, metabolic syndrome, diabetes, and chronic kidney disease, disordered TRLs and its remnants levels significantly increase the risk of atherosclerosis and cardiovascular disease development. Accumulation of over-synthesized TRLs in plasma, impaired function of enzymes involved in TRLs lipolysis, and impaired hepatic clearance of cholesterol-rich TRLs remnants can lead to arterial deposition of TRLs and its remnants, promoting foam cell formation and arterial wall inflammation. Therefore, understanding the pathogenesis of TRLs-induced AS and targeting it therapeutically could slow or impede AS progression, thereby reducing cardiovascular disease morbidity and mortality, particularly coronary atherosclerotic heart disease.