中等强度有氧运动通过NEAT1/SPI1/NLRP3通路改善急性冠脉综征斑块稳定性的机制研究

批准号:
81972143
项目类别:
面上项目
资助金额:
55.0 万元
负责人:
吴健
依托单位:
学科分类:
康复治疗与康复机制
结题年份:
2023
批准年份:
2019
项目状态:
已结题
项目参与者:
吴健
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中文摘要
易损斑块破裂是急性冠脉综合征(ACS)患者发生主要心脏不良事件的重要病理机制,而炎症激活是促使斑块不稳定的关键因素。抗炎治疗作为动脉粥样硬化新的治疗策略得到临床研究证实。基于运动作为潜在的抗炎工具的新概念,我们提出中等强度有氧运动通过抗炎作用稳定易损斑块从而改善ACS患者的预后。本课题组前期应用频域光学相干断层成像技术联合血管内超声研究发现中等强度有氧运动显著增加ACS患者易损斑块的稳定性,高通量测序发现运动后外周血巨噬细胞中长链非编码RNA NEAT1表达水平降低,且NEAT1作为长链非编码RNA参与巨噬细胞的自噬与极化。综上,我们首次提出中等强度有氧运动通过NEAT1/SPI1/NLRP3通路调控巨噬细胞功能发挥抗炎效果从而稳定易损斑块。本项目联合多学科,从临床出发,到细胞和动物水平揭示中等强度有氧运动通过抗炎作用稳定易损斑块的分子机制,为临床中等强度有氧运动治疗ACS患者提供新机制。
英文摘要
Vulnerable plaque rupture is the pathological mechanism of major adverse cardiac events (MACE) in patients with acute coronary syndrome (ACS). Activation of inflammatory is considered to be a key factor in promoting plaque formation and plaque instability. Anti-inflammatory treatment has been confirmed by clinical studies as a new treatment strategy. Based on the new concept of exercise as a potential anti-inflammatory therapeutic method, we suggest that moderate intensity aerobic exercise can improve clinical outcomes of ACS patients by stabilizing vulnerable plaques through anti-inflammatory effects. In our previous study, frequency domain optical coherence tomography combined with intravascular ultrasound showed that moderate intensity aerobic exercise increased the stability of vulnerable plaques in ACS patients. The high-throughput sequencing showed that the expression level of long non-coding RNA NEAT1 in peripheral blood mononuclear macrophages of patients undergone moderate intensity aerobic exercise was significantly reduced, and NEAT1 has involved in the autophagy and polarization of macrophages. In conclusion, we put forward for the first time that moderate intensity aerobic exercise regulates the function of macrophages through NEAT1/SPI1/NLRP3 pathway to exerts anti-inflammatory effect and stabilizes the vulnerable plaques. United with multiple disciplines, we revealed the molecular mechanism of moderate intensity aerobic exercises can stabilize vulnerable plaques through anti-inflammatory effect from the clinical point of view to the cytology and zoology levels. This specific molecular mechanism provides a new approach for the clinical treatment of ACS with moderate intensity aerobic exercise.
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专利列表
The lncRNA ANRIL regulates endothelial dysfunction by targeting the let-7b/TGF-βR1 signalling pathway
lncRNA ANRIL 通过靶向 let-7b/TGF-β R1 信号通路调节内皮功能障碍
DOI:10.1002/jcp.29993
发表时间:2020-08-11
期刊:JOURNAL OF CELLULAR PHYSIOLOGY
影响因子:5.6
作者:Liu, Xianglan;Li, Shufeng;Yu, Bo
通讯作者:Yu, Bo
DOI:10.1007/s00018-022-04331-0
发表时间:2022-05-22
期刊:Cellular and molecular life sciences : CMLS
影响因子:--
作者:
通讯作者:
DOI:10.1016/j.atherosclerosis.2023.05.009
发表时间:2023-05-26
期刊:ATHEROSCLEROSIS
影响因子:5.3
作者:Wang, Yanan;Chen, Liangqi;Yu, Bo
通讯作者:Yu, Bo
DOI:10.1161/atvbaha.123.319251
发表时间:2023-04
期刊:Arteriosclerosis, Thrombosis, and Vascular Biology
影响因子:--
作者:Qingyuan Yang;Shiliang Chen;Xingyi Wang;Xinyu Yang;Liangqi Chen;Tuo Huang;Yang Zheng;Xianghui Zhe
通讯作者:Qingyuan Yang;Shiliang Chen;Xingyi Wang;Xinyu Yang;Liangqi Chen;Tuo Huang;Yang Zheng;Xianghui Zhe
Circular RNA circSnx5 Controls Immunogenicity of Dendritic Cells through the miR-544/SOCS1 Axis and PU.1 Activity Regulation
环状 RNA circSnx5 通过 miR-544/SOCS1 轴和 PU.1 活性调节控制树突状细胞的免疫原性
DOI:10.1016/j.ymthe.2020.07.001
发表时间:2020-11-04
期刊:MOLECULAR THERAPY
影响因子:12.4
作者:Chen, Qi;Mang, Ge;Yu, Bo
通讯作者:Yu, Bo
有氧运动通过MeCP2乳酰化激活ZFP36转录促进TREM2hi巨噬细胞抗炎功能改善动脉粥样硬化的机制研究
- 批准号:82372565
- 项目类别:面上项目
- 资助金额:48万元
- 批准年份:2023
- 负责人:吴健
- 依托单位:
有氧运动通过Mettl14介导的m6A修饰调控巨噬细胞向Ly6Clow表型转化改善缺血性非梗阻冠心病的机制研究
- 批准号:--
- 项目类别:面上项目
- 资助金额:56万元
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- 依托单位:
miR-let-7i/E2F1/NEAT1前馈环调控tol-DC诱导心脏移植免疫耐受的机制
- 批准号:81670373
- 项目类别:面上项目
- 资助金额:57.0万元
- 批准年份:2016
- 负责人:吴健
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miR-let-7i靶向SOCS1通过TLR4信号通路调控树突细胞成熟诱导心脏移植免疫耐受机制
- 批准号:81200240
- 项目类别:青年科学基金项目
- 资助金额:23.0万元
- 批准年份:2012
- 负责人:吴健
- 依托单位:
国内基金
海外基金
