Cholesterol homeostasis plays a significant role in
cardiovascular disease. Previous studies have indicated that
ATP-binding cassette transporter A1 (ABCA1) is one of the most important
proteins that maintains
cholesterol homeostasis. ABCA1 mediates nascent
high-density lipoprotein biogenesis. Upon binding with
apolipoprotein A-I, ABCA1 facilitates the efflux of excess intracellular
cholesterol and
phospholipids and controls the rate-limiting step of reverse
cholesterol transport. In addition, ABCA1 interacts with the
apolipoprotein receptor and suppresses
inflammation through a series of signaling pathways. Thus, ABCA1 may prevent
cardiovascular disease by inhibiting
inflammation and maintaining
lipid homeostasis. Several studies have indicated that post-transcriptional modifications play a critical role in the regulation of ABCA1 transportation and plasma membrane localization, which affects its
biological function. Meanwhile, carriers of the loss-of-function ABCA1 gene are often accompanied by decreased expression of ABCA1 and an increased risk of
cardiovascular diseases. We summarized the ABCA1 transcription regulation mechanism, mutations, post-translational modifications, and their roles in the development of
dyslipidemia,
atherosclerosis,
ischemia/reperfusion, myocardial
infarction, and
coronary heart disease.