| Vol. 6.35 – 18 October, 2021 |
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| Scientists found that localized injuries, as experienced through exercise, activated a myofiber self-repair mechanism that was independent of satellite cells in mice and humans. [Science] |
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PUBLICATIONSRanked by the impact factor of the journal |
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| Researchers demonstrated that suppression of FGFR1 and OSMR by miR-1/133a was instrumental to prevent cardiomyocyte dedifferentiation and cell cycle entry in the adult heart. [Science Advances] |
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| Due to the role of methyltransferase-like 3 (METTL3) in the physiological proliferation of cardiomyocytes, investigators aimed to determine whether METTL3 could also promote cardiomyocyte proliferation under pathological conditions and to elucidate the underlying mechanism. [Cell Death Discovery] |
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| Rat primary cardiac fibroblasts were isolated and transformed into myofibroblasts using 5 ng/ml TGF-β1. Transformation of cells to myofibroblasts was confirmed with the presence of α-smooth muscle actin using Western blot. [Scientific Reports] |
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| Scientists described a mechanism by which mitochondrial-localized transcriptional co-repressor p107 regulated progenitors proliferation. They showed p107 directly interacted with the mitochondrial DNA, repressing mitochondrial-encoded gene transcription. [Nature Communications] |
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| Researchers showed that overexpression of miR-19b-3p in human skeletal muscle cells increased insulin signaling, glucose uptake, and maximal oxygen consumption, recapitulating the adaptive response to aerobic exercise training. [Nature Communications] |
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| Investigators reported that satellite cells, the stem cell population of adult skeletal muscle necessary for its growth and regeneration, expressed uniquely the longer NF-YA isoform, majorly associated with cell differentiation. [Nature Communications] |
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| Scientists used the YAC128 murine model of Huntington’s disease to examine the effects of mutant huntingtin on mitochondrial parameters related to aging in brain and skeletal muscle. [npj Aging and Mechanisms of Disease] |
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| Researchers showed a new method for automated engineering of 3D human skeletal muscle models in microplates and functional compound screening to address the lack of muscle wasting disease medication. [Communications Biology] |
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| Using human airway smooth muscle cells in culture as a model, the authors reported that activation of the cell surface β2-adrenoceptor, a Gs-coupled G protein-coupled receptor, evoked cAMP egress to the extracellular space. [American Journal of Respiratory and Critical Care Medicine] |
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| Researchers explored the effect of acetazolamide on various calcium-handling pathways in pulmonary arterial smooth muscle cells. [Pulmonary Circulation] |
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| Skeletal muscle contains a designated population of adult stem cells, called satellite cells, which are generally quiescent. The authors discuss the role and regulation of satellite cells in skeletal muscle homeostasis and regeneration. [Nature Reviews Molecular Cell Biology] |
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| Scientists summarize gene-editing, immunological and induced pluripotent stem cell based therapeutics for muscular dystrophy treatment. [European Journal of Pharmacology] |
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| Avidity Biosciences, Inc. announced that the US FDA has granted Fast Track Designation to its lead program, AOC 1001, for the treatment of myotonic dystrophy type 1. [Avidity Biosciences, Inc. (BioSpace, Inc.)] |
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| November 1 – 3, 2021 Virtual |
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| Baylor College of Medicine – Houston, Texas, United States |
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| Radboud University Medical Centre – Nijmegen, Netherlands |
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| Harvard Medical School – Boston, Massachusetts, United States |
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| Sanford Burnham Prebys Medical Discovery Institute – San Diego, California, United States |
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| European Centre Study Diabetes – Strasbourg, France |
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