Immune system-mediated atherosclerosis caused by deficiency of long non-coding RNA<i>MALAT1</i>in ApoE−/−<b>mice</b>

Abstract

The data suggest a molecular circuit involving the MALAT1-mascRNA system, interactions between MALAT1 and NEAT1, and key immune effector molecules, cumulatively impacting upon the development of atherosclerosis. It appears reasonable to look for therapeutic targets in this circuit and to screen for anomalies in the NEAT1-MALAT1 region in humans, too, as possible novel disease risk factors.