APOA1 (apolipoprotein A1) is the primary protein component of high-density lipoprotein (HDL) particles and functions as a master regulator of lipid and vascular homeostasis. Its primary role involves reverse cholesterol transport, whereby APOA1 promotes cholesterol efflux from peripheral tissues and acts as a cofactor for lecithin cholesterol acyltransferase (LCAT), facilitating cholesterol esterification and subsequent hepatic excretion 1. Beyond lipid metabolism, APOA1 exerts potent anti-inflammatory, anti-atherogenic, anti-apoptotic, and anti-thrombotic effects 1. Recent evidence reveals APOA1 modulates platelet function 2 and regulates matrix metalloproteinase-2 bioavailability through direct binding interactions 3. In pathological contexts, APOA1 dysfunction contributes to cardiovascular disease through multiple mechanisms. Proteolytic cleavage of APOA1 by asparagine endopeptidase at the N208 residue impairs HDL formation and cholesterol efflux, accelerating atherosclerosis development 4. Post-translational modifications of APOA1 by neutrophil myeloperoxidase generate immunogenic neo-epitopes that trigger proatherogenic IgG antibodies, predicting myocardial infarction and acute coronary syndrome risk 5. The APOA1 rs5069 polymorphism associates with early myocardial infarction susceptibility 6. Additionally, APOA1 depletion during sepsis severely compromises endothelial barrier integrity and microvascular perfusion 7, highlighting its critical protective role in vascular homeostasis. Therapeutic interventions including APOA1-mimetic peptides and synthetic reconstituted HDL are under clinical development 8.