代谢重编程在心房颤动发生中作用的研究进展

doi:10.16352/j.issn.1001-6325.2023.11.1718

基础医学与临床 ›› 2023, Vol. 43 ›› Issue (11): 1718-1722.doi: 10.16352/j.issn.1001-6325.2023.11.1718

代谢重编程在心房颤动发生中作用的研究进展

缪昊真, 陶磊, 宋冰洁, 张奇军^*

宁波大学附属人民医院心内科,浙江宁波 315000

收稿日期:2022-12-30 修回日期:2023-04-10 出版日期:2023-11-05 发布日期:2023-10-30
通讯作者: ^*rmzhangqijun@nbu.edu.cn
基金资助:
浙江省自然科学基金(LY20H020001);宁波市自然科学基金(2022J038)

Progress on the role of metabolic reprogramming in the occurrence of atrial fibrillation

MIAO Haozhen, TAO Lei, SONG Bingjie, ZHANG Qijun^*

Department of Cardiovascular Medicine, the Affiliated People's Hospital of Ningbo University, Ningbo 315000, China

Received:2022-12-30 Revised:2023-04-10 Online:2023-11-05 Published:2023-10-30
Contact: ^*rmzhangqijun@nbu.edu.cn

摘要/Abstract

摘要： 代谢重编程是细胞为满足能量需求,通过改变代谢模式促进细胞增殖,它的发生可以改变糖、氨基酸、脂肪酸的代谢模式,心房颤动是常见的心律失常之一,通过调控代谢重编程相关的途径可以有效的改善房颤的症状,降低房颤的易感性,以及提高患者的生存质量。

关键词: 心房颤动, 代谢组学, 代谢重编程

Abstract: Metabolic re-programming is a biological process which promotes cell proliferation by changing the metabolic mode to meet the energy demand. Its occurrence can change the metabolic mode of sugar, amino acid and fatty acid. Atrial fibrillation is one of the common arrhythmia. By regulating the pathway related to metabolic reprogramming may effectively alleviate the symptoms of atrial fibrillation, reduce the susceptibility of atrial fibrillation and improve the quality of life of patients.

Key words: atrial fibrillation, metabolomics, metabolic reprogramme

中图分类号:

R541.7

缪昊真, 陶磊, 宋冰洁, 张奇军. 代谢重编程在心房颤动发生中作用的研究进展[J]. 基础医学与临床, 2023, 43(11): 1718-1722.

MIAO Haozhen, TAO Lei, SONG Bingjie, ZHANG Qijun. Progress on the role of metabolic reprogramming in the occurrence of atrial fibrillation[J]. Basic & Clinical Medicine, 2023, 43(11): 1718-1722.

0
/ / 推荐

导出引用管理器 EndNote|Reference Manager|ProCite|BibTeX|RefWorks

链接本文: http://journal11.magtechjournal.com/Jwk_jcyxylc/CN/10.16352/j.issn.1001-6325.2023.11.1718

http://journal11.magtechjournal.com/Jwk_jcyxylc/CN/Y2023/V43/I11/1718

参考文献

[1]Hu B, Ge W, Wang Y, et al. Metabolomic and proteomic analyses of persistent valvular atrial fibrillation and non-valvular atrial fibrillation[J]. Front Genet, 2021,12:789485-789495.
[2]McCauley MD, Hong L, Sridhar A, et al. Ion channel and structural remodeling in obesity-mediated atrial fibrillation[J]. Circ Arrhythm Electrophysiol,2020,13:755-767.
[3]Shiou YL, Lin HT, Ke LY, et al. Very low-density lipoproteins of metabolic syndrome modulates STIM1, suppresses store-operated calcium entry, and deranges myofilament proteins in atrial myocytes[J]. J Clin Med, 2019,8:881-895.
[4]Lee HC, Shin SJ, Huang JK, et al. The role of postprandial very-low-density lipoprotein in the development of atrial remodeling in metabolic syndrome[J]. Lipids Health Dis, 2020,19:210-221.
[5]Harrison SL, Lane DA, Banach M, et al. Lipid levels, atrial fibrillation and the impact of age: results from the LIPIDOGRAM2015 study[J]. Atherosclerosis, 2020,312:16-22.
[6]Poulet C, Sanchez-Alonso J, Swiatlowska P, et al. Junctophilin-2 tethers T-tubules and recruits functional L-type calcium channels to lipid rafts in adult cardiomyocytes[J]. Cardiovasc Res, 2021,117:149-161.
[7]Tajik B, Tuomainen TP, Jarroch R, et al. Lipid levels, apolipoproteins, and risk of incident atrial fibrillation in men: a report from the kuopio ischaemic heart disease risk factor study (KIHD)[J]. J Clin Lipidol, 2022,16:447-454.
[8]Garg PK, Guan W, Nomura S, et al. Plasma omega-3 and omega-6 PUFA concentrations and risk of atrial fibrillation: the multi-ethnic study of atherosclerosis[J]. J Nutr, 2021;151:1479-1486.
[9]Tu T, Li B, Li X, et al. Dietary omega-3 fatty acids reduced atrial fibrillation vulnerability via attenuating myocardial endoplasmic reticulum stress and inflammation in a canine model of atrial fibrillation[J]. J Cardiol, 2022,79:194-201.
[10]Tajik B, Tuomainen TP, Isanejad M, et al. Serum n-6 polyunsaturated fatty acids and risk of atrial fibrillation: the kuopio ischaemic heart disease risk factor study[J]. Eur J Nutr, 2022,61:1981-1989.
[11]Zhang J, Zuo K, Fang C, et al. Altered synthesis of genes associated with short-chain fatty acids in the gut of patients with atrial fibrillation[J]. BMC Genomics, 2021,22:634-644.
[12]Zuo K, Fang C, Liu Z, et al. Commensal microbe-derived SCFA alleviates atrial fibrillation via GPR43/NLRP3 signaling[J]. Int J Biol Sci, 2022,18:4219-4232.
[13]Maria Z, Campolo AR, Scherlag BJ, et al. Dysregulation of insulin-sensitive glucose transporters during insulin resistance-induced atrial fibrillation[J]. Biochim Biophys Acta Mol Basis Dis, 2018,1864:987-996.
[14]Maria Z, Campolo AR, Scherlag BJ, et al. Insulin treatment reduces susceptibility to atrial fibrillation in type 1 diabetic mice[J]. Front Cardiovasc Med, 2020,7:134-146.
[15]Fu L, Rao F, Lian F, et al. Mechanism of electrical remodeling of atrial myocytes and its influence on susceptibility to atrial fibrillation in diabetic rats[J]. Life Sci, 2019,239:116903.doi:10.1016/j.Ifs.2019.116903.
[16]Zheng DL, Wu QR, Zeng P, et al. Advanced glycation end products induce senescence of atrial myocytes and increase susceptibility of atrial fibrillation in diabetic mice[J]. Aging Cell, 2022,21:e13734-e13746.
[17]Bohne LJ, Jansen HJ, Daniel I, et al. Electrical and structural remodeling contribute to atrial fibrillation in type 2 diabetic db/db mice[J]. Heart Rhythm, 2021,18:118-129.
[18]Wu X, Liu Y, Tu D, et al. Role of NLRP3-inflammasome/caspase-1/galectin-3 pathway on atrial remodeling in diabetic rabbits[J]. J Cardiovasc Transl Res, 2020,13:731-740.
[19]Wiersma M, van Marion DMS, Wust RCI, et al. Mitochondrial dysfunction underlies cardiomyocyte remodeling in experimental and clinical atrial fibrillation[J]. Cells, 2019,8:1202-1220.
[20]Yuan M, Gong M, He J, et al. IP3R1/GRP75/VDAC1 complex mediates endoplasmic reticulum stress-mitochondrial oxidative stress in diabetic atrial remodeling[J]. Redox Biol, 2022,52:102289-102302.
[21]Li J, Qi X, Ramos KS, et al. Disruption of sarcoplasmic reticulum-mitochondrial contacts underlies contractile dysfunction in experimental and human atrial fibrillation: a key role of mitofusin 2[J]. J Am Heart Assoc, 2022;11:e024478-e024496.
[22]Lu Han AW, Qing Li, Zhen Xia, et al. Homocysteine-induced electrical remodeling via the mediation of IP3R1Nav1.5 signaling pathway[J]. Am J Transl Res, 2020,12:3822-3841.
[23]Han L, Tang Y, Li S, et al. Protective mechanism of SIRT1 on hcy-induced atrial fibrosis mediated by TRPC3[J]. J Cell Mol Med, 2020,24:488-510.
[24]Lu C, Liu C, Mei D, et al. Comprehensive metabolomic characterization of atrial fibrillation[J]. Front Cardiovasc Med, 2022,9:911845-11863.
[25]Xie D, Xiong K, Su X, et al. Identification of an endogenous glutamatergic transmitter system controlling excitabi-lity and conductivity of atrial cardiomyocytes[J]. Cell Res, 2021;31:951-964.

代谢重编程在心房颤动发生中作用的研究进展

Progress on the role of metabolic reprogramming in the occurrence of atrial fibrillation

PDF

可视化

摘要/Abstract

引用本文

使用本文

参考文献

相关文章 9

编辑推荐

Metrics

本文评价

[1]	何丹, 阮中宝. 细胞外囊泡在心房颤动发病中的作用[J]. 基础医学与临床, 2022, 42(4): 671-674.
[2]	王玉敏, 陈济超, 王洪权, 王金华, 唐博. MicroRNAs靶向脂代谢重编程参与肝细胞癌发生的研究进展[J]. 基础医学与临床, 2022, 42(12): 1930-1934.
[3]	肖晓莲, 刘晓燕, 朱文凤, 杨晔宏, 杨俊涛, 孙伟. 尿液代谢组学非靶向质谱分析法两种采集模式的比较[J]. 基础医学与临床, 2021, 41(5): 729-734.
[4]	王诗淇, 赵蕾, 史晓光. 自身免疫性甲状腺炎小鼠的巨噬细胞极化失衡及代谢方式改变[J]. 基础医学与临床, 2021, 41(3): 340-345.
[5]	何权, 刘丹瑜, 叶君, 张艳丽, 朱华栋, 蒋澄宇, 徐军. 5-羟色胺对重症社区获得性肺炎严重程度的预测研究[J]. 基础医学与临床, 2020, 40(9): 1195-1200.
[6]	刘昕朋张斌. 细胞代谢组学研究方法和应用[J]. 基础医学与临床, 2019, 39(3): 414-418.
[7]	凌云钟国强李金轶何燕张景昌宋红星熊日新. 迷走神经与心房颤动犬上腔静脉肌袖内缝隙连接重构[J]. 基础医学与临床, 2010, 30(5): 510-514.
[8]	吴巧凤余曙光唐勇. 代谢组学及其在中医药领域的应用概况[J]. 基础医学与临床, 2009, 29(4): 443-445.
[9]	高崇瀚宋凌鲲李凡戴引殷跃辉. 甲状腺素对犬心房电生理特征和连接蛋白Cx43的影响[J]. 基础医学与临床, 2009, 29(10): 1092-1096.