New research reveals the role of noncoding genes in atherogenesis

About 75% of human genome does not have the function of coding protein However, these noncoding regions of the genome are not simply "junk" sequences Recently, Professor Mark Feinberg and others in the Department of cardiovascular medicine of Harvard University revealed the role of non coding genes in the formation of atherosclerosis Atherosclerosis is a kind of heart disease, which is caused by the hardening and narrowing of blood vessels, the obstruction of blood flow In this study, Feinberg and his colleagues used a preclinical atherosclerotic model to discover the role of a long non coding RNA (lncrna) in the pathogenesis of atherosclerosis, which may indicate the direction of new therapies for atherosclerosis The results were published in the journal Science Translational Medicine "We have found new factors that control vascular wall aging, which are not traditional genes or proteins, but are part of a non coding sequence," Feinberg said We have a lot of discoveries about the importance of cholesterol and inflammation in heart disease, and this new discovery makes us need to carefully consider how non coding genes affect the occurrence of cardiovascular disease and whether we can develop new treatments " Feinberg and colleagues used an atherosclerotic mouse model in which the mice began to develop atherosclerotic lesions at 12 weeks The researchers isolated RNA from the innermost layer of the vessel wall and looked at the expression of the entire genome to find out which genes changed in activity during disease progression or regression Finally, the author found the most active gene, snhg12, which encodes long-chain RNA molecules but not proteins The RNA molecule has been found in a variety of species including humans, pigs and mice In order to better understand the role of snhg12, the researchers conducted some experiments to artificially reduce or improve the activity of the RNA molecule They found that decreased snhg12 activity led to increased atherosclerosis, but more snhg12 significantly reduced the progression of the disease In order to understand the mechanism of snhg12, the authors try to find the downstream interaction molecules The results showed that snhg12 could interact with a molecule involved in DNA damage repair and aging process If this interaction is destroyed, the walls of the blood vessels leak and lead to the accumulation of bad cholesterol In the end, the small molecules that promote DNA damage repair can inhibit the development of atherosclerosis, indicating the potential therapeutic approach Original title: scitransmed: new research reveals the relationship between aging and atherosclerosis