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Front Biosci (Landmark Ed). 2017 Jan 1;22:48-65.

MicroRNA regulation of autophagy in cardiovascular disease.

Author information

1
Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio 43210, USA.
2
Department of Pharmacology, The Penn State Hershey Cancer Institute, The Pennsylvania State University, College of Medicine and Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA.
3
Department of Surgery, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, Columbus, Ohio 43210, USA, Hua.Zhu@osumc.edu.

Abstract

Autophagy, a form of lysosomal degradation capable of eliminating dysfunctional proteins and organelles, is a cellular process associated with homeostasis. Autophagy functions in cell survival by breaking down proteins and organelles and recycling them to meet metabolic demands. However, aberrant up regulation of autophagy can function as an alternative to apoptosis. The duality of autophagy, and its regulation over cell survival/death, intimately links it with human disease. Non-coding RNAs regulate mRNA levels and elicit diverse effects on mammalian protein expression. The most studied non-coding RNAs to-date are microRNAs (miRNA). MicroRNAs function in post-transcriptional regulation, causing profound changes in protein levels, and affect many biological processes and diseases. The role and regulation of autophagy, whether it is beneficial or harmful, is a controversial topic in cardiovascular disease. A number of recent studies have identified miRNAs that target autophagy-related proteins and influence the development, progression, or treatment of cardiovascular disease. Understanding the mechanisms by which these miRNAs work can provide promising insight and potential progress towards the development of therapeutic treatments in cardiovascular disease.

PMID:
27814601
PMCID:
PMC5349319
[Indexed for MEDLINE]
Free PMC Article

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