Small molecules, big effects: the role of microRNAs in regulation of cardiomyocyte death
MicroRNAs (miRNAs) are a class of small non-coding RNAs involved in posttranscriptional regulation of gene expression, and exerting regulatory roles in plethora of biological processes. In recent years, miRNAs have received increased attention for their crucial role in health and disease, including...
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Published in: | Cell death & disease Vol. 5; no. 7; p. e1325 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
London
Nature Publishing Group UK
01-07-2014
Springer Nature B.V Nature Publishing Group |
Subjects: | |
Online Access: | Get full text |
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Summary: | MicroRNAs (miRNAs) are a class of small non-coding RNAs involved in posttranscriptional regulation of gene expression, and exerting regulatory roles in plethora of biological processes. In recent years, miRNAs have received increased attention for their crucial role in health and disease, including in cardiovascular disease. This review summarizes the role of miRNAs in regulation of cardiac cell death/cell survival pathways, including apoptosis, autophagy and necrosis. It is envisaged that these miRNAs may explain the mechanisms behind the pathogenesis of many cardiac diseases, and, most importantly, may provide new avenues for therapeutic intervention that will limit cardiomyocyte cell death before it irreversibly affects cardiac function. Through an in-depth literature analysis coupled with integrative bioinformatics (pathway and synergy analysis), we dissect here the landscape of complex relationships between the apoptosis-regulating miRNAs in the context of cardiomyocyte cell death (including regulation of autophagy–apoptosis cross talk), and examine the gaps in our current understanding that will guide future investigations. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-3 content type line 23 ObjectType-Review-1 ObjectType-Article-1 ObjectType-Feature-2 These two authors contributed equally to this work. |
ISSN: | 2041-4889 2041-4889 |
DOI: | 10.1038/cddis.2014.287 |