Depleted Long Non-Coding RNA Sox2ot Suppresses Oxidative Stress and Inflammation of Vascular Smooth Muscle Cells Through microRNA-145-Targeted Egr1 in Abdominal Aortic Aneurysm

2019 ◽  
Author(s):  
Huyu Lin ◽  
Bin You ◽  
Xiaohu Wang ◽  
Dongsheng Zhou ◽  
Zhiqun Chen ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Non Coding Rna ◽  
Abdominal Aortic ◽  
Long Non Coding Rna

scholarly journals Vascular Smooth Muscle Cells in Aortic Aneurysm: From Genetics to Mechanisms

2021 ◽  
Author(s):  
Haocheng Lu ◽  
Wa Du ◽  
Lu Ren ◽  
Milton H. Hamblin ◽  
Richard C. Becker ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Abdominal Aortic Aneurysm ◽  
Aortic Aneurysm ◽  
Vascular Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Vascular Smooth Muscle Cells ◽  
Thoracic Aortic Aneurysm ◽  
Muscle Cells ◽  
Abdominal Aortic ◽  
Aneurysm Development

Abstract Aortic aneurysm, including thoracic aortic aneurysm and abdominal aortic aneurysm, is the second most prevalent aortic disease following atherosclerosis, representing the ninth‐leading cause of death globally. Open surgery and endovascular procedures are the major treatments for aortic aneurysm. Typically, thoracic aortic aneurysm has a more robust genetic background than abdominal aortic aneurysm. Abdominal aortic aneurysm shares many features with thoracic aortic aneurysm, including loss of vascular smooth muscle cells (VSMCs), extracellular matrix degradation and inflammation. Although there are limitations to perfectly recapitulating all features of human aortic aneurysm, experimental models provide valuable tools to understand the molecular mechanisms and test novel therapies before human clinical trials. Among the cell types involved in aortic aneurysm development, VSMC dysfunction correlates with loss of aortic wall structural integrity. Here, we discuss the role of VSMCs in aortic aneurysm development. The loss of VSMCs, VSMC phenotypic switching, secretion of inflammatory cytokines, increased matrix metalloproteinase activity, elevated reactive oxygen species, defective autophagy, and increased senescence contribute to aortic aneurysm development. Further studies on aortic aneurysm pathogenesis and elucidation of the underlying signaling pathways are necessary to identify more novel targets for treating this prevalent and clinical impactful disease.

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