Articles tagged with Myoblasts
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Researchers found that the tenascin-C protein promotes a thriving community of functional muscle stem cells needed for efficient muscle regeneration. Aging reduces skeletal muscle regeneration due to lower levels of TnC and impaired muscle stem cell function.
Scientists have discovered that MYOD protein can act as a gene silencer, clearing out old 'furniture' to reset the cell's identity. This finding challenges dogma and opens up new avenues for understanding cellular reprogramming and regenerative medicine therapies.
A new study reveals that myosin binding protein-C (cMyBP-C) is essential for regulating cardiac muscle contraction, particularly under increased stress. The protein's absence or mutation can lead to diseases such as heart failure and hypertropic cardiomyopathy.
A team from Tokyo Metropolitan University has successfully implanted myoblasts onto healthy muscle in mice using an extracellular matrix scaffold. This breakthrough treatment could treat ageing-related muscular atrophy without scarring, offering a promising avenue for regenerative medicine.
Researchers at the University of Houston College of Pharmacy discovered key mechanisms of skeletal muscle regeneration and growth following resistance exercise. Increasing levels of Inositol-requiring enzyme 1 (IRE1) or X-box binding protein 1 (XBP1) in muscle stem cells may improve muscle repair and reduce disease severity.
Researchers develop nanofibrous matrices containing MXene nanoparticles to aid in muscle regeneration. The study reveals molecular mechanisms behind the effects of MXene nanoparticles on muscle growth, suggesting a promising avenue for treating volumetric muscle loss and muscle-related ailments.
Scientists at the Terasaki Institute for Biomedical Innovation have developed a new bioink that enhances the formation of mature skeletal muscle tissue from muscle precursor cells, increasing efficiency and potential therapies for muscle loss or injury. The bioink's sustained delivery of IGF-1 promotes muscle regeneration and repair.
Researchers found that metformin + leucine (MET+LEU) treatment prevents myotube atrophy by reversing cellular senescence and improving proteostasis. The study used C2C12 myoblasts, aged mouse single myofibers, and human primary myotubes to demonstrate MET+LEU's skeletal muscle cell-autonomous properties.
Researchers from Tokyo Metropolitan University have discovered a protein called PDGF-B that not only promotes muscle growth but also enhances myotube maturation, leading to increased contractile strength. The findings offer a game-changing approach to treating muscle injuries and atrophy.
Researchers at the University of Montreal discovered a key mechanism in muscle regeneration, enabling targeted therapies for diseases like muscular dystrophy. By biasing the conformation of a protein called ELMO2, they improved muscle fusion and regeneration in mouse models.
Researchers at Tokyo Metropolitan University discovered that a protein excreted by type I muscle fibers can differentiate surrounding myoblasts into type I fibers, upending the notion that fiber ratios are fixed at birth. This finding has significant implications for treating conditions such as type 2 diabetes and aging populations.
Researchers uncover the pleiotropic functions of hnRNPK in regulating skeletal muscle cell differentiation, including inhibition of myoblast differentiation and suppression of genes involved in endoplasmic reticulum stress. The study suggests that targeting hnRNPK could be a potential therapeutic strategy for treating human disorders.
The study of MUNC long non-coding RNA reveals the importance of experimentally determining its structure to identify functional domains. The researchers found that two structural domains, including six common 'hairpins,' were crucial for regulating gene expression and muscle cell differentiation.
Researchers found that oligo DNA promotes muscle differentiation and reduces inflammation in myoblasts, exacerbating diabetes. This discovery holds potential for developing a therapeutic agent to treat muscle wasting associated with various diseases.
Researchers identified a novel oligo-DNA molecule that induces myoblast differentiation, potentially treating muscle atrophy and related diseases. The 'myogenetic oligo-DNA' (myoDN) acts as an aptamer, binding to protein nucleolin and activating the p53 signaling pathway.
Researchers at the University of Montreal have discovered two proteins essential to the development of skeletal muscle. The study, published in Nature Communications, sheds light on the 'dance' of muscle cell movement and how cells fuse together to form a single large cell, leading to improved understanding of rare muscular diseases.
Researchers at UofL discovered the critical role of MyD88 in muscle development and regeneration, highlighting its potential to improve therapies for degenerative muscle disorders. The study also suggests that increasing MyD88 levels could inhibit growth of rhabdomyosarcomas and enhance engraftment of exogenous myoblasts.
Johns Hopkins researchers have engineered human muscle cells bearing genetic mutations from people with Duchenne muscular dystrophy (DMD), enabling the study of genetic variations among patients. The cells can also be used to test new therapies and may hold potential for genetic correction and transplantation.
Researchers used electron microscopy to study the dynamic process of myoblast fusion with muscle cells, revealing a series of distinct stages that require communication between transmembrane elements and actin cytoskeleton. The study provides insights into understanding muscle development and repair processes in vertebrates.
Researchers discovered that muscle cells in developing fly embryos send 'finger-like' protrusions into neighboring cells to facilitate fusion. The actin-rich fingers help form a small pore connecting the two cell types, eventually fusing them together.
Research suggests FHL1 enhances transcription factor NFATc1 activity to promote muscle hypertrophy. Overexpressing FHL1 in mice and myoblasts resulted in increased strength and endurance.
The SEISMIC study found that injecting muscle cells into scarred areas of the heart improved patients' symptoms, including increased walking distance, but did not improve heart function or size. Researchers concluded that cell therapy is feasible and may provide symptom relief for heart failure patients.
Researchers identify protein WIP as crucial for cell fusion, shedding light on muscle development; potential applications include regenerating muscle tissue with stem cells. The study's findings have implications for understanding various cellular processes and may lead to new treatments or therapies.
Scientists have identified two microRNAs, miR-1 and miR-133, that play opposing roles in determining whether myoblasts proliferate or differentiate into mature muscle cells. Increasing miR-1 promotes differentiation, while increasing miR-133 enhances proliferation.
The FKHR gene helps myoblasts fuse into muscles, but a deficiency contributes to muscle cancer. FKHR's dual role is regulated by different processes depending on the cell context.
Researchers have found that deacetylase inhibitors enhance muscle gene expression and formation in human and mouse myoblasts. This discovery may lead to methods to induce muscle growth, regeneration, and repair in adults with muscular dystrophy.