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Optical Coherence Tomography Based Biomechanical Fluid-Structure Interaction Analysis of Coronary Atherosclerosis Progression
Published on: January 15, 2022
Long non-coding RNAs in coronary atherosclerosis
Yiran Wang1, Xianjing Song1, Zhibo Li1
1Department of Cardiology, The Second Hospital of Jilin University, Changchun, Jilin 130021, China.
Insights
Long non-coding RNAs (lncRNAs) are crucial in coronary atherosclerosis (CAS) development. Understanding lncRNA roles in CAS pathogenesis offers new prevention and treatment strategies for this cardiovascular disease.
Area of Science:
- Cardiovascular Biology
- Molecular Medicine
- Atherosclerosis Research
Background:
- Coronary atherosclerosis (CAS) is a primary cause of global mortality, characterized by complex pathogenesis involving dyslipidemia, metabolic dysfunction, and inflammation.
- Endothelial cell (EC) injury and subsequent inflammatory responses are key initiating factors in CAS development.
- The intricate mechanisms underlying CAS necessitate research into vascular cell dysfunction, metabolic disorders, and immune responses.
Purpose of the Study:
- To review the significant role of non-coding RNAs, particularly long non-coding RNAs (lncRNAs), in the pathogenesis of coronary atherosclerosis (CAS).
- To explore the regulatory functions of lncRNAs in the progression of CAS.
- To discuss the potential of lncRNAs in the prevention and treatment strategies for CAS.
Main Methods:
- Literature review focusing on non-coding RNAs and their involvement in cardiovascular disease.
- Analysis of current research on lncRNA functions in the context of CAS pathogenesis.
- Synthesis of findings related to lncRNA mechanisms in endothelial dysfunction, lipid metabolism, and inflammatory pathways.
Main Results:
- lncRNAs are increasingly recognized as critical regulators in the complex pathogenesis of CAS.
- Specific lncRNAs influence key processes such as EC injury, VSMC proliferation, and inflammatory signaling in CAS.
- Dysregulation of lncRNAs contributes to the development and progression of coronary atherosclerosis.
Conclusions:
- lncRNAs represent a promising area for understanding CAS mechanisms.
- Targeting lncRNAs may offer novel therapeutic avenues for preventing and treating coronary atherosclerosis.
- Further investigation into lncRNA functions is essential for advancing cardiovascular disease management.
Abstract:
Coronary atherosclerosis (CAS), a leading cause of cardiovascular disease, is a major cause of death worldwide. CAS is a chronic disease in the aorta that can be caused by dyslipidemia, abnormal glucose metabolism, endothelial cell dysfunction, vascular smooth muscle cell (VSMC) or fibrous connective tissue hyperplasia, immune inflammatory reactions, and many other factors. The pathogenesis of CAS is not fully understood, as it is a complex lesion complicated by multiple factors. Damage-response theories have put forward endothelial cell (EC) injury as the initiating factor for CAS; the addition of lipid metabolism disorders may enhance monocyte adhesion, increase the proliferation and migration of fibroblasts and VSMCs, and accelerate the development of CAS. Furthermore, inflammatory and immune responses can create a vicious cycle of endothelial injury, which also plays key roles in the formation of CAS. Therefore, in order to elucidate the mechanisms controlling CAS, it is important to study the etiology of vascular cell dysfunction, abnormal energy and metabolism disorders, and immune and inflammatory reactions. Non-coding RNAs play regulatory roles in the pathogenesis of CAS, especially long non-coding RNAs (lncRNAs); lncRNAs have recently become a major focus for cardiovascular disease mechanisms, as they play numerous roles in the progression of CAS. Therefore, in this review, we discuss the role of lncRNAs in the pathogenesis of coronary CAS, and their role in the prevention and treatment of coronary CAS.
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