| Vol. 6.00 – 4 January, 2021 |
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| By employing the human embryonic stem cell (hESC) to cardiomyocyte differentiation system and generating QKI-deficient hESCs using CRISPR/Cas9 gene editing technology, scientists analyzed the physiological role of QKI in cardiomyocyte differentiation, maturation, and contractile function. [Nature Communications] |
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| PUBLICATIONSRanked by the impact factor of the journal |
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| Investigators showed that the transcription factor zinc finger E-box-binding homeobox 2 (ZEB2) was increased in stressed cardiomyocytes and induced a cardioprotective cross-talk between cardiomyocytes and endothelial cells to enhance angiogenesis after ischemia. [Nature Communications] |
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| Despite the absence of AT1A receptors in cardiomyocytes, C-SMKOs developed robust cardiac hypertrophy. By contrast, R-SMKOs developed identical levels of hypertrophy in response to pressure overload–induced by transverse aortic banding. [Hypertension] |
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| Researchers explored the role of miRNA and autophagy in hypoxia/reoxygenation (H/R)-induced cardiomyocyte injury. Cardiomyocyte H9c2 was exposed to H/R to simulate H/R injury in vitro. [Human Cell] |
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| The authors investigated the in vitro role of microRNA-520d-3p in human myocardial cell myocardial H/R injury. [Journal of Thrombosis and Thrombolysis] |
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| Scientists used gelatin methacryloyl (GelMA) laden with C2C12 cells. The cells in the GelMA fiber were exposed to electrical stimulation, which induced cell alignment. Various cellular activities, such as cell viability, cell guidance, and proliferation/myogenic differentiation of the microfibrous cells in GelMA, were investigated in response to parameters. [Theranostics] |
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| Researchers identified peroxisome proliferator-activated receptor gamma (PPARγ) as a negative regulator of miR-29b, a microRNA that is able to promote multiple types of muscle atrophy. Suppression of miR-29b prevented angiotensin II-induced muscle atrophy both in vitro and in vivo. [Molecular Therapy-Nucleic Acids] |
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| The authors investigated the effects of puromycin‐sensitive aminopeptidase (PSA) on C2C12 myoblast proliferation and differentiation by knocking down PSA. Aminopeptidase enzymatic activity was reduced in PSA‐knockdown myoblasts. [Journal of Cellular Physiology] |
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| Researchers tested whether a laminin 111‐rich extracellular matrix could affect smooth muscle cells (SMCs) phenotype and differentiation status. Using time lapse microscopy, image analyses, qRT‐PCR, immunohistochemistry and immunoblotting, and transmission electron microscopy, they showed that SMCs acquired a migratory behavior with a decreased expression of differentiation markers and relocation of FAK. [Cell Biology International] |
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| The authors discuss the overlapping post-transcriptional regulatory pathways that mediate muscle development, how these pathways are disrupted in neuromuscular disorders, and advances in RNA-mediated therapies that present a novel approach to the treatment of these diseases. [Trends in Molecular Medicine] |
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| Scientists discuss recent findings on the roles of cellular metabolism in determining skeletal stem cell fate, coordinating osteoblast and chondrocyte function, and organizing stromal support of hematopoiesis. [Nature Metabolism] |
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| Audentes Therapeutics announced that the FDA has lifted the clinical hold for the ASPIRO clinical trial evaluating AT132 in patients with X-linked myotubular myopathy. [Audentes Therapeutics] |
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| February 3 – 23, 2021 Virtual |
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| Hannover Medical School – Hannover, Germany |
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| University of California, Los Angeles – Los Angeles, California, United States |
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| Mayo Clinic – Rochester, Minnesota, United States |
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| Stanford University – Stanford, California, United States |
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| National Institute of Arthritis and Musculoskeletal and Skin Diseases – Washington, DC, United States |
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