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MicroRNAs in Cardiac Autophagy: Small Molecules and Big Role

Key Laboratory of Cellular Physiology, Ministry of Education, Department of Physiology, Shanxi Medical University, Taiyuan 030001, China
Institute for Translational Medicine, Qingdao University, Qingdao 266021, China
Author to whom correspondence should be addressed.
Cells 2018, 7(8), 104;
Received: 5 July 2018 / Revised: 8 August 2018 / Accepted: 9 August 2018 / Published: 11 August 2018
(This article belongs to the Special Issue Regulatory microRNA)
Autophagy, which is an evolutionarily conserved process according to the lysosomal degradation of cellular components, plays a critical role in maintaining cell homeostasis. Autophagy and mitochondria autophagy (mitophagy) contribute to the preservation of cardiac homeostasis in physiological settings. However, impaired or excessive autophagy is related to a variety of diseases. Recently, a close link between autophagy and cardiac disorders, including myocardial infarction, cardiac hypertrophy, cardiomyopathy, cardiac fibrosis, and heart failure, has been demonstrated. MicroRNAs (miRNAs) are a class of small non-coding RNAs with a length of approximately 21–22 nucleotides (nt), which are distributed widely in viruses, plants, protists, and animals. They function in mediating the post-transcriptional gene silencing. A growing number of studies have demonstrated that miRNAs regulate cardiac autophagy by suppressing the expression of autophagy-related genes in a targeted manner, which are involved in the pathogenesis of heart diseases. This review summarizes the role of microRNAs in cardiac autophagy and related cardiac disorders. Furthermore, we mainly focused on the autophagy regulation pathways, which consisted of miRNAs and their targeted genes. View Full-Text
Keywords: microRNAs; autophagy; mitophagy; cardiac diseases; biomarker microRNAs; autophagy; mitophagy; cardiac diseases; biomarker
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MDPI and ACS Style

Sun, T.; Li, M.-Y.; Li, P.-F.; Cao, J.-M. MicroRNAs in Cardiac Autophagy: Small Molecules and Big Role. Cells 2018, 7, 104.

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