What is it about?
Arsenic trioxide (ATO) is a known anti-acute promyelocytic leukemia (APL) reagent, whose clinical applications are limited by its serious cardiac toxicity and fatal adverse effects, such as sudden cardiac death resulting from long QT syndrome (LQTS). The mechanisms of cardiac arrhythmia due to ATO exposure still need to be elucidated. Long non-coding RNAs (lncRNAs) are emerging as major regulators of various pathophysiological processes. This study aimed to explore the involvement of lncRNAs in ATO-induced LQTS in vivo and in vitro.
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Why is it important?
To our knowledge, this report is the first to demonstrate that lncRNA Kcnq1ot1 downregulation is responsible for QT interval prolongation induced by ATO at least partially by repressing Kcnq1 expression. lncRNA Kcnq1ot1 has important pathophysiological functions in the heart and could become a novel antiarrhythmic target.
Perspectives
The discovery of lncRNA Kcnq1ot1-mediated effects on cardiac rhythm in ATO-induced LQTS not only proposes a therapeutic target for ameliorating the cardiac toxicity of ATO but also provides a novel strategy for the treatment of arrhythmias and other related diseases.
Yanan Jiang
Harbin Medical University
Read the Original
This page is a summary of: Downregulation of Long Non-Coding RNA Kcnq1ot1: An Important Mechanism of Arsenic Trioxide-Induced Long QT Syndrome, Cellular Physiology and Biochemistry, January 2018, Karger Publishers,
DOI: 10.1159/000486357.
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