Non-coding RNAs in cardiac regeneration

Lichan Tao, Yihua Bei, Yanli Zhou, Junjie Xiao and Xinli Li _

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Oncotarget. 2015; 6:42613-42622. https://doi.org/10.18632/oncotarget.6073

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Lichan Tao1,*, Yihua Bei2,3,*, Yanli Zhou1, Junjie Xiao2,3 and Xinli Li1

1 Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, China

2 Regeneration and Ageing Lab, Experimental Center of Life Sciences, School of Life Science, Shanghai University, Shanghai, China

3 Shanghai Key Laboratory of Bio-Energy Crops, School of Life Science, Shanghai University, Shanghai, China

* These authors have contributed equally to this work

Correspondence to:

Xinli Li, email:

Junjie Xiao, email:

Keywords: non-coding RNA, cardiac regeneration, microRNA, long non-coding RNA

Received: August 09, 2015 Accepted: September 28, 2015 Published: October 10, 2015


Developing new therapeutic strategies which could enhance cardiomyocyte regenerative capacity is of significant clinical importance. Though promising, methods to promote cardiac regeneration have had limited success due to the weak regenerative capacity of the adult mammalian heart. Non-coding RNAs (ncRNAs), including microRNAs (miRNAs, miRs) and long non-coding RNAs (lncRNAs), are functional RNA molecules without a protein coding function that have been reported to engage in cardiac regeneration and repair. In light of current regenerative strategies, the regulatory effects of ncRNAs can be categorized as follows: cardiac proliferation, cardiac differentiation, cardiac survival and cardiac reprogramming. miR-590, miR-199a, miR-17-92 cluster, miR302-367 cluster and miR-222 have been reported to promote cardiomyocyte proliferation while miR-1 and miR-133 suppress that. miR-499 and miR-1 promote the differentiation of cardiac progenitors into cardiomyocyte while miR-133 and H19 inhibit that. miR-21, miR-24, miR-221, miR-199a and miR-155 improve cardiac survival while miR-34a, miR-1 and miR-320 exhibit opposite effects. miR-1, miR-133, miR-208 and miR-499 are capable of reprogramming fibroblasts to cardiomyocyte-like cells and miR-284, miR-302, miR-93 , miR-106b and lncRNA-ST8SIA3 are able to enhace cardiac reprogramming. Exploring non-coding RNA-based methods to enhance cardiac regeneration would be instrumental for devising new effective therapies against cardiovascular diseases.

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