Long noncoding RNAs: Important participants and potential therapeutic targets for myocardial ischaemia reperfusion injury

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 po...

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Veröffentlicht in:Clinical and experimental pharmacology & physiology 2020-11, Vol.47 (11), p.1783-1790
Hauptverfasser: Ding, Yu‐Ming, Chan, Elsa Ching, Liu, Li‐Chang, Liu, Zhi‐Wei, Wang, Qiong, Wang, Jian‐Li, Cui, Xiao‐Pei, Jiang, Fan, Guo, Xiao‐Sun
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Sprache:eng
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Zusammenfassung: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. We provide an updated summary on contributions of lncRNAs to the development of myocardial ischaemia reperfusion injury, with an emphasis on the functional links between several well established cardiac lncRNAs and regulation of cellular outcomes post I/R.
ISSN:0305-1870
1440-1681
1440-1681
DOI:10.1111/1440-1681.13375