Abstract
Alpha-1 antitrypsin deficiency patients (AATD) have lower risk of myocardial infarction, a cardiovascular disease that is related to increased remnant cholesterol levels, but not to low-density lipoprotein (LDL) levels. However, when AAT is knocked out in mice (AAT-KO), inflammatory-related, cholesterol metabolism-related, and lipid metabolism-related gene expression in mouse liver was increased, and these data support previous evidence from clinic patients and from a small clinical trial that AAT is in negative feedback regulation with LDL. Herein is a brief summary to examine the roles of AAT in these overlapping pathways.
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