Proper muscle function constitutes a precondition for good heath and an active lifestyle during an individual's lifespan and any deviations from normal skeletal muscle development and its functions may lead to numerous health conditions including e.g. myopathies and increased mortality. It is thus not surprising that there is an increasing need for understanding skeletal muscle developmental processes and the associated molecular pathways, especially as such information could find further uses in therapy. The understanding of complex skeletal muscle developmental networks was broadened with the discovery of microRNA (miRNA) molecules. MicroRNAs are evolutionary conserved small non-coding RNAs capable of negatively regulating gene expression on a post-transcriptional level by means of miRNA-mRNA interaction. Several miRNAs expressed exclusively in muscle have been labeled myomiRs. MyomiRs represent an integral part of skeletal muscle development, i.e. playing a significant role during skeletal muscle proliferation, differentiation and regeneration. The purpose of this review is to provide a summary of current knowledge regarding the involvement of myomiRs in the individual phases of myogenesis and other aspects of skeletal muscle biology, along with an up-to-date list of myomiR target genes and their functions in skeletal muscle and miRNA-related therapeutic approaches and future prospects.
BackgroundDespite the widespread use of implantable cardioverter‐defibrillators (ICDs) in clinical practice, concerns exist regarding ICD lead durability. The performance of specific lead designs and factors determining this in large populations need clarification.Methods and ResultsThe Medline, Embase, and Cochrane Collaboration databases were searched for studies including ≥2 of the most commonly implanted leads. The Mantel‐Haenszel random‐effects model was used. Seventeen studies were selected, including a total of 49 871 patients—5538 implanted with Durata (St. Jude Medical Inc), 10 605 with Endotak Reliance (Boston Scientific), 16 119 with Sprint Quattro (Medtronic Corp), 11 709 with Sprint Fidelis (Medtronic Corp), and 5900 with Riata (St. Jude Medical Inc)—with follow‐up of 136 509 lead‐years. Although the Durata lead presented a numerically higher rate, no statistically significant differences in the mean incidence of lead failure (0.29%–0.45% per year) were observed in comparison of the 3 nonrecalled leads. A higher event rate was documented with the Riata (1.0% per‐year increase) and Sprint Fidelis (>2.0% per‐year increase) leads compared with nonrecalled leads. An indication of increased incidence of Durata lead failure versus Sprint Quattro and Endotak Reliance leads was observed in 1 of 3 included studies, allowing for comparison of purely electrical lead failure, but this requires further evaluation.ConclusionsEndotak Reliance (8F), Sprint Quattro (8F), and Durata (7F) leads displayed low annual incidence of failure; however, long‐term follow‐up data are still scarce. More data are needed to clarify the performance and safety of the Durata lead.
Hypertension is the most common adverse effect of the inhibitors of vascular endothelial growth factor (VEGF) pathway-based therapy (VEGF pathway inhibitors therapy, VPI therapy) in cancer patients. VPI includes monoclonal antibodies against VEGF, tyrosine kinase inhibitors, VEGF Traps, and so-called aptamers that may become clinically relevant in the future. All of these substances inhibit the VEGF pathway, which in turn causes a decrease in nitric oxide (NO) and an increase in blood pressure, with the consequent development of hypertension and its final events (e.g., myocardial infarction or stroke). To our knowledge, there is no current study on how to provide an optimal therapy for patients on VPI therapy with hypertension. This review summarizes the roles of VEGF and NO in vessel biology, provides an overview of VPI agents, and suggests a potential treatment procedure for patients with VPI-induced hypertension.
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