Articles tagged with Muscle Cells
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A new UTSA study has redefined the role of a cell's cytoskeleton, finding it plays a crucial part in energy transfer and information processing within neurons. This breakthrough challenges traditional views of the cytoskeleton's primary function in supporting cellular structure.
Researchers discovered that neutrophils can induce a previously unrecognized type of cell death in tissues, leading to the destabilization of atherosclerotic plaques. This process causes inflammation, which increases the likelihood of plaque rupture and subsequent cardiovascular events.
Researchers have mapped the structure of a chloride channel in muscle cells, providing new information on its regulation. The findings may lead to more efficient drug development for neuromuscular diseases such as ALS and SMA.
Researchers found that pericyte transplantation can facilitate full regrowth of muscle fibers in skeletal muscle following limb immobilization. Pericytes play a crucial role in regulating muscle mass, particularly in the context of recovery from disuse atrophy.
A study of elite female weightlifters found they have the same amount and in some cases more fast twitch fibers than their male counterparts. This challenges a persistent stereotype about women athletes and highlights the influence of training on muscle fiber development.
Scientists at Duke-NUS Medical School have made a breakthrough in heart muscle regeneration by priming stem cells to become heart tissues. The novel method uses the laminin protein to promote differentiation of human embryonic stem cells into cardiovascular precursor cells, which can then differentiate into cardiac muscle fibers.
Researchers at Penn State and the University of Alabama developed a technique to spin starch fibers using Lego pieces, creating potential scaffolds for lab-grown 'clean' meat. The starch fiber mats have been optimized for better alignment and strength, making them suitable for biomedical applications.
Researchers found that IgG antibodies play a crucial role in stabilizing arterial plaques, reducing the risk of rupture and clotting. The study suggests that these antibodies may be a new target for mitigating atherosclerosis and improving cardiovascular health.
Researchers discovered that muscle stem cells produce proteins MyoD and Hes1 in an oscillatory manner, ensuring a sufficient supply of stem cells. This phenomenon is crucial for muscle regeneration and differentiation. The study aims to develop new therapies for muscular disorders by understanding the oscillation mechanism.
A University of Minnesota Medical School research breakthrough highlights the potential of cell therapies for treating muscular dystrophy. The study identifies the molecular signature of muscle stem cells generated in vitro and their transformation upon transplantation into mice with muscular dystrophy.
A study published in The Journal of Bone & Joint Surgery found that rotator cuff muscle stem cells have a higher propensity to develop into fat cells, leading to fatty infiltration and weakening of the muscles. This genetic basis may explain why rotator cuff tears are difficult to rehabilitate.
Researchers have found that nuclei gained during training persist even when muscle cells shrink due to disuse or disease, allowing for rapid growth when retrained. This discovery has important implications for public health policy and suggests that exercise in early life can help prevent frailty in old age.
Researchers at the University of Illinois have developed a method to engineer muscle tissue that integrates with neurons, enabling functional and responsive muscle. The approach uses grooved platforms to promote ordered muscle fiber growth and neuronal integration.
Researchers at Rutgers University have developed a new model of cardiac muscle cells that can pump together, potentially treating heart failure. The newly created cardiac muscle cells were made to work cohesively through the over-expression of a protein called CREG.
Researchers precisely cut a widespread DNA region from the genome using genome editing, revealing its role in cardiovascular disease. The 9p21.3 haplotype causes abnormalities in vascular smooth muscle cells, leading to heart attacks and stroke. This breakthrough may lead to new treatments for millions worldwide.
Scientists identified a key player in blood pressure regulation, PKD2 channel, which regulates blood vessel constriction and relaxation. The study found that switching off PKD2 reduces blood pressure in mice, indicating potential as a new drug target for treating high blood pressure.
Scientists have discovered a way to detect the early signs of atherosclerosis, leading to blocked arteries, by analyzing changes in blood vessel cells. The study used single-cell RNA-sequencing and lineage labelling to identify unusual cells that express stem cell genes, which could help diagnose and treat cardiovascular diseases.
Researchers found that vamorolone improved muscle repair and strength in experimental models of LGMD2B, while prednisolone worsened muscle weakness and degeneration. The study suggests modified steroids like vamorolone may be an option for some patients with the disease.
Researchers at Georgia Institute of Technology developed a molecular matrix that effectively delivers muscle satellite cells to injured muscle tissue, promoting healing and protection from immune reactions. The hydrogel therapy has potential to treat muscular dystrophy patients, including those with Duchene muscular dystrophy.
Researchers have discovered a nematode worm that develops similar nerve damage to humans when exposed to mutated TTR proteins. The C. elegans model allows scientists to study the molecular mechanisms of TTR-linked diseases and potentially develop new treatments.
A team of researchers found that LYVE-1 macrophages protect arteries from becoming stiff by interacting with smooth muscle cells and reducing collagen production. The protein is responsible for binding to hyaluronan, facilitating the degradation of collagen.
Researchers discovered fibro-adipogenic progenitor cells promote muscle wasting and scarring in spinal cord injury, ALS, and SMA models. By targeting IL-6-STAT3 signaling, they found a potential new avenue for treating or testing motor neuron diseases.
Researchers identify myofibroblasts as key players in activating nucleus movement, potentially leading to new therapeutic strategies for muscle disorders. The discovery could improve understanding of muscle differentiation, functionality, and regeneration.
Scientists successfully regenerate skeletal muscle cells in mice with muscular dystrophy by using cells from animal teratomas. The study showed improved potential with 80% regeneration compared to the current 5-10%.
A study published in Proceedings of the National Academy of Sciences reveals how gene defects lead to congenital heart defects. The researchers found that the absence of the CHD4 protein allows for the production of abnormal, 'hybrid' muscle cells that cannot pump blood efficiently.
Researchers from Penn Medicine identified a new target for treating heart failure by reversing the stiffness of diseased heart muscle cell struts, which can improve the beating strength of cells isolated from transplant patients. The team aims to develop therapies that seek out damaged cellular struts to reverse their harmful influence.
A new gene therapy approach has shown dramatic reduction of post-infarction arrhythmias in mice by electrically coupling non-excitable cells to undamaged heart cells. The treatment involves introducing a single gene, Connexin43, which bridges the conduction block in damaged hearts.
Researchers successfully convert mature skin cells into immature muscle cells using a simple approach, promoting muscle regeneration in injured mice. The induced myogenic progenitor cells (iMPCs) engrafted in damaged tissue and contributed to sustained muscle regeneration.
Researchers at San Francisco State University have discovered a breakthrough technique for testing AMPK protein levels in human muscle cells. This innovative approach allows for precise analysis of individual muscle fibers, enabling better understanding of how the body regulates blood sugar levels.
Researchers found that exercising mice produced over four and a half times more new heart muscle cells than sedentary counterparts. The study suggests exercise can stimulate the heart to regenerate tissue after a heart attack.
Researchers have identified a new gene, ari-1, linked to aortic aneurysms in humans through a fruit fly study. The study found that mutations in the ari-1 gene disrupt mechanical sensing mechanisms in the body, leading to abnormal nuclei shapes and potentially contributing to the development of aortic aneurysms.
Researchers at University of Illinois Chicago developed chimeric cells that can restore the structural muscle protein dystrophin in people with Duchenne muscular dystrophy, potentially avoiding the need for immunosuppressive drugs.
Researchers found that aging muscle shows decreased sensitivity to ADP, resulting in higher levels of reactive oxygen species (ROS) and degenerative loss of muscle mass. Despite exercise resistance training, there were no improvements in age-associated cellular stress.
Researchers at the University of California, Berkeley, found that brown fat cells can be activated to burn calories when stimulated, similar to how muscle cells work. The team identified a potential pathway to trigger this activation and hopes to develop drugs to stimulate brown fat function.
Researchers found diverse landscape of gene expression changes across all cell types in visual cortex, involving 611 genes linked to neural connectivity. The study suggests that each cell has a unique genetic program tailored to its function within the neural circuit.
A research team led by Dr. Ralf Gilsbach and Prof. Dr. Lutz Hein from the University of Freiburg has mapped out the gene regulators in the DNA of human cardiac muscle cells for the first time. They discovered over 100,000 gene switches that control gene activity, providing insight into mechanisms misdirected in heart disease.
Researchers at Queen Mary University of London discovered a new mechanism by which heart cells sense stiffness, involving both contraction forces and resting tension. The study found increased resting tension in heart cells after a heart attack or disease, leading to abnormal mechanosensing and signalling that contributes to heart fail...
A study published in European Journal of Nutrition found that dietary isoflavone aglycone can reduce muscle atrophy by blocking the apoptosis-dependent pathway in muscle fibers. The researchers observed significantly thicker muscle fibers in mice fed with AglyMax supplement compared to those on a normal diet.
Infections with MRSA bacteria appear to permanently compromise the lymphatic system, impairing its ability to pump lymphatic fluid. This impairment may contribute to frequent recurrences of MRSA infection in patients.
Duke researchers successfully grew functioning human skeletal muscle from induced pluripotent stem cells, offering a promising path for cellular therapies, drug discovery, and studying rare diseases. The technique allows for the growth of far more muscle cells and provides an easier route to genome editing and individualized models.
Rhabdomyosarcoma, the most prevalent soft tissue cancer in children, arises from immature progenitor cells that would normally develop into blood vessel cells, not muscle cells. The discovery opens a path for better treatments and may lead to new therapeutic drug targets.
Scientists have made breakthroughs in understanding the early stages of CAVD by studying pig valves and creating a lab model. They found that certain sugar molecules called glycosaminoglycans (GAGs) can increase blood vessel growth, but also trap low-density lipoprotein (LDL) molecules.
Researchers at UCLA have successfully created skeletal muscle from human pluripotent stem cells, a major step towards developing a cell replacement therapy for Duchenne Muscular Dystrophy. The study uses natural human development as a guide to mature muscle cells in the lab and restore dystrophin-producing muscle fibers.
Congenital myotonic dystrophy (CDM) is characterized by progressive muscle wasting and weakness. Researchers have identified an upregulation of the interleukin-6 (IL-6) myokine signaling pathway in CDM muscles, suggesting that enhanced RNA toxicity contributes to severe CDM phenotypes through aberrant IL-6 signaling.
Scientists show that transplanted muscle cells loaded with magnetic nanoparticles engraft better onto the existing tissue, leading to improved heart function. The technology could potentially be used to revitalize damaged heart tissue and has shown promising results in mice.
Researchers studied 3000 human neuromuscular junctions, revealing details of their anatomy and structure. Human NMJs were found to be smaller and frailer than those in mice and rats, with no effect of age on their health.
Researchers at Technical University of Munich discovered that lower levels of microRNA 29 suppresses cardiac fibrosis, contradicting previous studies. The study highlights potential new approaches for developing drugs against fibrotic diseases, particularly in treating cardiac fibrosis.
A team of researchers discovered that different subtypes of muscle cells play critical roles in orchestrating tissue regeneration in flatworms. Removing specific muscle groups was shown to disrupt the regeneration process, revealing essential functions for longitudinal and circular fibers.
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.
Researchers found that massage increased muscle growth after loss and improved protein manufacture in cells, leading to faster regeneration. Additionally, non-massaged muscles showed accelerated growth, suggesting massage could benefit both injured and healthy limbs.
The Max Delbrück Center receives funding to collaborate on the Human Cell Atlas project, focusing on understanding heart muscle cells. The goal is to create a three-dimensional model of the human heart and advance personalized medicine.
A Penn study suggests that DNA 3D packaging controls which genes are available for activation, influencing cell differentiation. The researchers found that tethering DNA to the nuclear periphery with an epigenetic enzyme contributes to a cell becoming a certain type.
Researchers found that low dietary potassium promotes elevated aortic stiffness, while increased dietary potassium alleviates it. Increased potassium also reduced vascular calcification and aortic stiffness in mouse models, suggesting its potential to protect against heart disease.
Researchers have confirmed that cartilaginous fish fin and hypobranchial muscles develop via a similar mechanism to limb muscles in land-dwelling vertebrates and bony fish. Conserved genes, including Pax3 and Myod, were also identified.
A synthetic DNA-targeting molecule called PIP-S2 has been developed to guide human induced pluripotent stem cells into specific cell types. This breakthrough overcomes challenges in current approaches and offers a promising strategy for tissue regeneration.
Portuguese researchers have discovered how cellular nuclei reach their position within muscle cells, a process disrupted in most muscle disorders. This finding has important implications for developing novel therapeutic strategies to treat muscular diseases and sport-induced muscle injuries.
Reactive oxygen species are crucial signals that start muscle repair processes. Proper mitochondrial function is necessary for energy production and repairing injured myofibers. Excess antioxidants can inhibit this signaling process, exacerbating muscle damage.
A new study found that poor nitric acid responsiveness may lead to arteriovenous fistula failure in hemodialysis patients. Researchers discovered that improving nitric oxide responsiveness through manipulation of local mediators can prevent fistula maturation failure and potentially improve patient outcomes.
Researchers found that elevated levels of protein Cdk8 in heart muscle cells lead to declining heart function and heart failure. The study suggests modifying gene expression may provide a path to preventive treatments for heart failure.
Researchers at UNC and NC State found that acetylation promotes TDP-43 clumping in animals, leading to muscle degeneration. In mouse models, reversing protein clumping prevented sIBM-related muscle weakness, offering potential therapy reversal.