miRNA调节心肌肥厚的关键因子 | 实验室临床技术导航

途径基因组以旁激素方式即刻成甲状腺粗大的时有发生。科学研究推测肝病甲状腺病中所浸润的肝细胞必须激素含硫miR-155的外泌体，并通过如此一来抗病毒下转调FoxO3a基因组隐含，转管控甲状腺细胞焦亡和粗大。相反在肝病甲状腺病激素假设中所基因组隐含敲低miR-155可正向更高水准的FoxO3a亚基隐含，下转调细胞焦亡多种类型caspase-1、IL-1β、IL-18和焦亡的执行分子会GSDMD亚基隐含；显著降低心正BMI比、降低甲状腺粗大区域，提高肺脏系统 [47] 。

对于miR-155的科学研究上会非甲状腺基因组隐含的miRNA在甲状腺细胞中所的少量隐含也必须直接影响甲状腺解构全过程。即使非甲状腺或甲状腺大脑皮层中所的miRNA通过旁激素的方式也可投身于转管控甲状腺解构。

知晓miRNA在甲状腺解构全过程中所更多的基因组隐含生物学多种类型，不仅帮助解释了甲状腺解构的时有发生拓展必要，也为甲状腺解构临床研究与放射治疗提供了新的基本系统。尽管以外miRNA作为甲状腺解构生物学多种类型带有良好的应用前景，基于miRNA投递的甲状腺解构放射治疗也先取入到临床研究之前，但是仍需要实质性的透彻探索，以筛选出更具基因组隐含的生物学多种类型，降低放射治疗所带来的不良反应，助益甲状腺解构的预防、临床研究和放射治疗。（知晓其他miRNA对甲状腺解构的转管控，点选“阅读标题”，先取讲座读标题！）

【参考文献】

[1] Chen C，Ponnusamy M， Liu C，et al. MicroRNA as a therapeutic target in cardiac remodeling[J] Bio Res internat, 2017, 2017: 1278436.

[2] Stroynowska-Czerwinska A,Fiszer A,Krzyzosiak WJ. The panorama of miRNA-mediated mechanisms in mammalian cells[J] Cellular and molecular life sciences : CMLS, 2014, 71(12): 2253-70.

[3] Romaine SP, Tomaszewski M,Condorelli G,et al. MicroRNAs in cardiovascular disease: an introduction for clinicians[J] Heart (British Cardiac Society), 2015, 101(12): 921-8.

[27] Molkentin JD, Lu JR, Antos CL,et al. A calcineurin-dependent tranional pathway for cardiac hypertrophy[J] Cell, 1998, 93(2): 215-28.

[28] keda S, He A, Kong SW,et al. MicroRNA-1 negatively regulates expression of the hypertrophy-associated calmodulin and Mef2a genes[J] Mol Cell Biol, 2009, 29(8): 2193-204.

[29] Elia L, Contu R,Quintalle M,et al. Reciprocal regulation of microRNA-1 and insulin-like growth factor-1 signal transduction cascade in cardiac and skeletal muscle in physiological and pathological conditions[J] Circulation, 2009, 120(23): 2377-85.

[30] Hua Y, Zhang Y, Ren J. IGF-1 deficiency resists cardiac hypertrophy and myocardial contractile dysfunction: role of microRNA-1 and microRNA-133a[J] J Cell Mol Med, 2012, 16(1): 83-95.

[31] Li Q, Song XW, Zou J,et al. Attenuation of microRNA-1 derepresses the cytoskeleton regulatory protein twinfilin-1 to provoke cardiac hypertrophy[J] J Cell Sci, 2010, 123(Pt 14): 2444-52.

[36] Li Y, Liang Y,Zhu Y,et al. Noncoding RNAs in cardiac hypertrophy[J] J Card Translat Res, 2018, 11(6): 439-49.

[37] Li Q, Lin X, Yang X,et al. NFAT is negatively regulated in miR-133a-mediated cardiomyocyte hypertrophic repression[J] Amer J Physiol Heart Circulat Physiol, 2010, 298(5): H1340-7.

[38] Dong DL, Chen C, Huo R, et al. Reciprocal repression between microRNA-133 and calcineurin regulates cardiac hypertrophy: a novel mechanism for progressive cardiac hypertrophy[J] Hypertension (Dallas, Tex : 1979), 2010, 55(4): 946-52.

[39] Callis TE, Pandya K, Seok HY, et al. MicroRNA-208a is a regulator of cardiac hypertrophy and conduction in mice[J] J Clini Investigat, 2009, 119(9): 2772-86.

[40] van Rooij E, Sutherland LB, Qi X,et al. Control of stress-dependent cardiac growth and gene expression by a microRNA[J] Science (New York, NY), 2007, 316(5824): 575-9.

[41] Montgomery RL, Hullinger TG,Semus HM, et al. Therapeutic inhibition of miR-208a improves cardiac function and survival during heart failure[J] Circulation, 2011, 124(14): 1537-47.

[42] Toyoda M, Shirato H, Nakajima K, et al. jumonji downregulates cardiac cell proliferation by repressing cyclin D1 expression[J] Developmental cell, 2003, 5(1): 85-97.

[43] Seok HY, Chen J,Kataoka M, et al. Loss of MicroRNA-155 protects the heart from pathological cardiac hypertrophy[J] Circulat Res, 2014, 114(10): 1585-95.

[47] Wang B, Wang ZM,Ji JL,et al. Macrophage-Derived Exosomal Mir-155 Regulating Cardiomyocyte Pyroptosis and Hypertrophy in Uremic Cardiomyopathy[J] JACC Basic to translational science, 2020, 5(2): 148-66.

-End-

编辑 | 骆秉涵 王迪

标题以《miRNA在甲状腺解构中所的依赖性性与临床研究诊疗价值》大篇幅发表在《临床研究实验室》杂志2022年5月刊讲座“分子会临床研究”实验室临床研究技术导航版块

本文转载自其他其网站，不代表肥胖界观点和见解。如有内容和图片的著作权异议，请及时联系我们（电话号码：guikequan@hmkx.cn）

。

胸腔镜手术伤口恢复图
飞秒手术后能用海露玻璃酸钠滴眼液吗
宝宝消化不良怎么办
中高考期间肠胃功能失调怎么办
双醋瑞因胶囊几天一个疗程
新冠阳性吃什么药效果最好
新冠特效药有哪些
消化不良想吐怎么办
腰疼吃什么药物治疗
服用完蒙脱石散可以喝酒吗