Non-coding RNA-linked epigenetic regulation in cardiac hypertrophy.

Non-coding RNA-linked epigenetic regulation in cardiac hypertrophy.
复制标题

心脏肥大中非编码RNA相关的表观遗传调控

DOI:
10.7150/ijbs.26215
复制
发表时间:
2018
影响因子:
9.2
通讯作者:
Wang K
Wang K
中科院分区:
生物学2区
文献类型:
--
作者:
Dong Y;Xu S;Liu J;Ponnusamy M;Zhao Y;Zhang Y;Wang Q;Li P;Wang K

文献摘要

参考文献

被引文献

相似文献

心肌肥厚是心肌对各种病理性损伤引起的压力超负荷的适应性扩张,伴随着一系列复杂的信号通路的改变。在肥大过程中,许多变化发生在细胞水平,包括基因重编程关闭染色质调节。近十年来的研究表明,异常的表观遗传修饰,如DNA甲基化、组蛋白修饰、核酸氧化修饰等,可导致染色体结构改变和心功能障碍。越来越多的证据表明,非编码RNA(non-coding RNAs,ncRNA)在心脏病理过程中对基因表达具有重要的调控作用。新出现的证据表明ncRNA可能作为改变染色质状态的信号,然而,有关心脏病理中ncRNA相关的表观遗传调控机制的知识仍然很大程度上未被探索。在这篇综述中,我们总结了目前的信息之间的关联ncRNA和表观遗传修饰在心脏肥大,我们已经讨论了他们的串扰。此外,这篇综述提供了深入了解他们的治疗和诊断潜力,用于治疗肥厚性心脏病。
Cardiac hypertrophy is an adaptive enlargement of myocardium in response to pressure overload caused various pathological insults, which is accompanied by alteration of a complex cascade of signaling pathways. During the hypertrophy process, many changes occur at cellular level including gene reprogramming by turning off chromatin regulators. Studies from the past decade have demonstrated that the abnormal epigenetic modifications, such as DNA methylation, histone modification, and oxidative modification of nucleic acid, could lead to changes in chromosome structure and cardiac dysfunction. Increasing evidence indicates that non-coding RNAs (ncRNAs) have functional significance in modulating the gene expression during those pathological events in the heart. Emerging evidences have highlighted that ncRNAs might serve as a signal for changing the state of chromatin, however, the knowledge about the ncRNA-linked epigenetic regulatory mechanisms in cardiac pathologies is still largely unexplored. In this review, we summarize the current information on association between ncRNAs and epigenetic modifications in cardiac hypertrophy, and we have discussed their crosstalk. In addition, this review provides insights into their therapeutic and diagnostic potential for treating hypertrophic heart disease.
DOI: 10.1161/01.cir.0000441139.02102.80
发表时间: 2014-01-21
期刊: Circulation
影响因子: 37.8
作者:
Go AS;Mozaffarian D;Roger VL;Benjamin EJ;Berry JD;Blaha MJ;Dai S;Ford ES;Fox CS;Franco S;Fullerton HJ;Gillespie C;Hailpern SM;Heit JA;Howard VJ;Huffman MD;Judd SE;Kissela BM;Kittner SJ;Lackland DT;Lichtman JH;Lisabeth LD;Mackey RH;Magid DJ;Marcus GM;Marelli A;Matchar DB;McGuire DK;Mohler ER 3rd;Moy CS;Mussolino ME;Neumar RW;Nichol G;Pandey DK;Paynter NP;Reeves MJ;Sorlie PD;Stein J;Towfighi A;Turan TN;Virani SS;Wong ND;Woo D;Turner MB;American Heart Association Statistics Committee and Stroke Statistics Subcommittee
通讯作者: American Heart Association Statistics Committee and Stroke Statistics Subcommittee
DOI: 10.1016/j.bbamcr.2016.03.005
发表时间: 2016-07
期刊: Biochimica et biophysica acta
影响因子: --
作者:
Chang CP;Han P
通讯作者: Han P
DOI: 10.1161/circulationaha.116.024171
发表时间: 2017-08-22
期刊: CIRCULATION
影响因子: 37.8
作者:
Heggermont, Ward A.;Papageorgiou, Anna-Pia;Heymans, Stephane
通讯作者: Heymans, Stephane
DOI: 10.1152/ajpheart.00149.2014
发表时间: 2014-07-15
影响因子: 4.8
作者:
Demos-Davies, Kimberly M.;Ferguson, Bradley S.;McKinsey, Timothy A.
通讯作者: McKinsey, Timothy A.
DOI: 10.1016/j.cell.2007.01.043
发表时间: 2007-03-23
期刊: CELL
影响因子: 64.5
作者:
Brennecke, Julius;Aravin, Alexei A.;Hannon, Gregory J.
通讯作者: Hannon, Gregory J.