Abstract
Cardiac Ca2+ cycling and signaling are closely associated with cardiac function. Changes in cellular Ca2+ homeostasis may lead to aberrant cardiac rhythm and may play a critical role in the pathogenesis of cardiac diseases, due to their exacerbation of heart failure. MicroRNAs (miRNAs) play a key role in the regulation of gene expression at the post-transcriptional level and participate in regulating diverse biological processes. The emerging evidence indicates that the expression profiles of miRNAs vary among human diseases, including cardiovascular diseases. Cardiac Ca2+-handling and signaling proteins are also regulated by miRNAs. Given the relationship between cardiac Ca2+ homeostasis and signaling and miRNA, Ca2+-related miRNAs may serve as therapeutic targets during the treatment of heart failure. In this review, we summarize the knowledge currently available regarding the role of Ca2+ in cardiac function, as well as changes in Ca2+ cycling and homeostasis and the handling of these processes by miRNAs during cardiac ischemia-reperfusion injury.
Highlights
Myocardial ischemia-reperfusion (I/R) injury is one of the leading causes of heart failure, and the signs and symptoms of I/R injury are characterized by an insufficient supply of oxygen and nutrients to the body; slowed, asynchronous contraction; and impaired relaxation of the heart muscle [1,2]
Altered expression and activity of Ca2+-related proteins are associated with cardiac dysfunction, which is observed in many patients with heart failure [3,4]
Wang et al demonstrated that cardiac-specific overexpression of miR-494 in transgenic mice heart improves the recovery of cardiac function, reduces myocardial infarction size and prevents apoptosis by targeting the proapoptotic proteins PTEN, ROCK1, and CaMKIIδ, as well as antiapoptotic proteins FGFR2 and LIF, and via the subsequent activation of AKT signaling in mitochondria [72]
Summary
Myocardial ischemia-reperfusion (I/R) injury is one of the leading causes of heart failure, and the signs and symptoms of I/R injury are characterized by an insufficient supply of oxygen and nutrients to the body; slowed, asynchronous contraction; and impaired relaxation of the heart muscle [1,2]. The guide strand is the functional strand of the mature miRNAs and negatively regulates gene expression either by inhibiting mRNA translation or inducing mRNA degradation, which results from the complete or incomplete binding to the 3'. A number of miRNAs have been discovered; a small portion of miRNAs are known to be expressed in the heart and an even smaller portion of miRNAs have been identified to be related to cardiac Ca2+ homeostasis [11]. Given the relationship between intracellular Ca2+ homeostasis and miRNAs during the regulation of cardiac function, the ability of miRNAs to regulate Ca2+-handling proteins may be an important therapeutic target in the treatment of heart disease [1,14,15,16].
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