| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 5905082 | Gene | 2016 | 6 Pages |
â¢Atherosclerosis is a chronic disease of the arterial wall and a leading cause of death worldwide. We found that molecular pathways underlying plaque formation in atherosclerosis were related to immune response, angiogenesis, cell proliferation, apoptosis and hypoxia microenvironment, suggesting that the pathophysiology of atherosclerosis are multiple processes.â¢Three lnc-RNAs, GAS5, SNHG6 and Zfas1 were significantly increased in the plaque of atherosclerosis patients compared to normal people. A complex interaction of mRNA and lncRNA was identified in atherosclerosis.â¢Our results provide a global transcriptomic network of atherosclerosis development in rats and possible targets that could lead to new clinical applications in future.
Atherosclerosis is a chronic disease of the arterial wall and a leading cause of death worldwide. Though the pathophysiology of atherosclerotic lesion formation has been studied, we still lack evidence of the global changes in the artery during atherosclerosis. In this report, we induced atherosclerosis in rats and conducted GeneChip analysis on carotid arteries with or without plaque formation. We found that molecular pathways underlying plaque formation in atherosclerosis were related to immune response, angiogenesis, cell proliferation, apoptosis and hypoxic microenvironments, suggesting that the pathophysiology of atherosclerosis is varied. In addition, we showed that three lncRNAs, GAS5, SNHG6 and Zfas1, were significantly increased in the plaque of atherosclerosis patients compared to normal people. A complex interaction of mRNA and lncRNA was identified in atherosclerosis. Our results provide a global transcriptomic network of atherosclerosis development in rats and possible targets that could lead to new clinical applications in the future.
