Recent studies have indicated miR-33a/b regulate genes involved in cholesterol and fatty acid metabolism pathways. miR-33a/b strongly represses the cholesterol transporter ABCA1, resulting in decreased generation of HDL-C and reverse cholesterol transport. In addition, miR-33a/b also inhibit key genes involved in fatty acid metabolism resulting in the accumulation of triglycerides. The ability to inhibit miR-33a/b to reverse these events provides a novel therapeutic approach to correct dyslipidemia and metabolic syndrome.
"This study represents a significant advance from our proof-of-concept studies in mice showing that anti-miR-33 can both raise HDL and improve existing atherosclerotic vascular disease," said Katey Rayner, PhD in the Department of Medicine at NYU Langone Medical Center and co-author of the study. "These exciting results now bring the use of miR-33 inhibitors one step closer to the clinic."
Source: NYU Langone Medical Center / New York University School of Medicine