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Long noncoding RNAs: Important participants and potential therapeutic targets for myocardial ischaemia reperfusion injury
Author(s) -
Ding YuMing,
Chan Elsa Ching,
Liu LiChang,
Liu ZhiWei,
Wang Qiong,
Wang JianLi,
Cui XiaoPei,
Jiang Fan,
Guo XiaoSun
Publication year - 2020
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/1440-1681.13375
Subject(s) - autophagy , reperfusion injury , ischemia , myocardial ischemia , long non coding rna , coronary artery disease , myocardial ischaemia , homeostasis , apoptosis , ischemic injury , disease , medicine , biology , bioinformatics , rna , microbiology and biotechnology , cardiology , gene , genetics
Myocardial ischaemia reperfusion (I/R) injury is one of the leading causes of coronary artery disease‐associated morbidity and mortality. While different strategies have been used to limit I/R injuries, cardiac functions often do not recover to the normal level as anticipated. Recent studies have pointed to important roles of long noncoding RNAs (lncRNAs) in the development of myocardial I/R injury. LncRNA is a class of RNA molecules of more than 200 nucleotides in length which are not translated into proteins. I/R causes dysregulation of lncRNA expression in cardiomyocytes, thereby affecting multiple cellular functions including mitochondrial homeostasis, apoptosis, necrosis and autophagy, suggesting that manipulating lncRNAs may be of great potential in counteracting I/R injury‐induced myocardial dysfunctions. In this review, we provide an updated summary on our knowledge about contributions of lncRNAs to the development of I/R injury, with an emphasis on the functional links between several well established cardiac lncRNAs and regulation of cellular outcomes post I/R.