Articles tagged with Muscle Cells
A recent study suggests that successful genetic blueprints for mesodermal development are recycled by evolution, rather than being invented anew in different species. The researchers found highly conserved transcription factor binding sites across six fruit fly species, indicating a shared regulatory program.
Researchers found that blocking the action of a signaling protein in cardiac muscle cells halted serious ill effects of high blood pressure on the heart, including enlargement and scar tissue formation. Further tests revealed potential new treatments for heart failure by targeting specific proteins involved in disease progression.
A study published in Biophysical Journal discovers a state of cardiac muscle with low metabolic rate, which may help regulate energy use and promote efficiency in the heart. This finding suggests that therapeutic interventions increasing the population of this state could be cardio-protective during times of stress.
Researchers at the National Institute of Arthritis and Musculoskeletal and Skin Diseases have identified a key player in muscle repair: the gene Ezh2. By activating this gene, satellite cells may proliferate and compensate for underlying defects, potentially increasing quality of life for individuals with degenerative diseases.
An international team of scientists used a powerful synchrotron X-ray technique to observe muscle protein changes inside intact and contracting muscle cells. The results revealed the conformation of myosin molecular motors in resting muscles and the signalling pathway between actin and myosin filaments.
Researchers developed a chemical cocktail to convert mouse muscle fibers into cells that form the first stages of regenerating limbs. The methods have implications for regenerative medicine and stem cell biology, potentially speeding wound healing and creating new tissues.
A new study reveals that free radicals act as signal substances that increase the heart's contractions with the correct force. Persistent stress can lead to chronic levels of free radicals, potentially contributing to heart failure.
Muscle cell fusion is a previously thought to be mutually consented event, but research reveals it's actually an invasive battle where one cell forces the other using finger-like projections.
Pitt researchers have successfully grown arteries with high elasticity using baboon smooth muscle cells, containing 20% of the protein elastin found in natural arteries. The process resembles how it would be used in a patient and has the potential to overcome a major barrier to creating living-tissue replacements for damaged arteries.
A new mouse model of Duchenne muscular dystrophy suggests that muscle stem cells are key to understanding the disease's progression. The research found that mice with a similar mutation to humans experience severe muscle weakness and shortened life spans due to the inability of their muscle stem cells to keep up with ongoing damage.
Researchers at Tel Aviv University have created a new computer method to measure mechanical stress in fat cells, which can help control the amount of fat produced by these cells. The study has direct applications in weight loss programs, treating bedsores, and managing chronic diabetes.
Researchers found that moderate alcohol consumption inhibits notch, preventing buildup of smooth muscle cells in blood vessels and contributing to narrowed arteries. This discovery could lead to the development of a new treatment for heart disease.
Researchers discovered a genetic material involved in regulating HDL cholesterol levels. A microRNA called miR-33a helps keep high-density lipoprotein stable, and inhibiting it may raise HDL levels. Additionally, biopolymer hydrogel injections improved heart function and quality of life in heart failure patients.
Researchers used Canada's national centre for synchrotron research to build a high-resolution model of the ryanodine receptor. This sheds new light on life-threatening congenital heart conditions and could lead to developing new treatments to prevent calcium leakage.
A recent study has revealed a model for understanding Facioscapulohumeral Muscular Dystrophy (FSHD), which is linked to the generation of toxic RNA that damages muscle cells. Variations in chromosome 4 play a crucial role in this process, and researchers have identified potential new treatments by silencing the effects of this RNA.
Engineers and physicians at the University of Washington have developed a scaffold that supports the growth and integration of stem cell-derived cardiac muscle cells. The scaffold accelerates oxygen and nutrient supply to transplanted tissue, promoting heart repair and vascular tissue engineering.
Researchers at Stanford University School of Medicine successfully replicated the ability of newts to regenerate tissue in mouse cells by blocking the expression of two tumor-suppressing proteins. This breakthrough may lead to future regenerative therapies for humans, and could involve sending us back down the evolutionary tree.
Scientists studying sea squirts have found a connection between the heart's second field and lower jaw muscles, suggesting an evolutionary link between these two structures. This discovery could provide clues about how complex hearts evolved in humans.
Researchers are developing a method to identify and purify stem cells from patients themselves that can give rise to beating heart cells. This approach aims to create an ideal product for transplant to repair heart damage caused by heart attack or cardiomyopathy.
Researchers have discovered a new source of stem cells that can form heart muscle cells, which can help repair damaged hearts. The stem cells, called human amniotic membrane-derived mesenchymal cells (hAMCs), were obtained from the amniotic membrane and showed promising results in laboratory studies.
University of Missouri researchers have documented satellite cell movements and behaviors using time-lapse photography. Understanding the interactions between these cells and their 'host' myofiber may help overcome obstacles to gene therapies for muscular dystrophy.
A team of researchers from Université Laval has proven that it is possible to repair the defective gene responsible for Duchenne muscular dystrophy. They developed enzymes called meganucleases that can correct the dystrophin gene and restore its expression in muscle cells.
Researchers at U-M have solved a long-standing mystery about how insulin-like growth factors (IGFs) work on muscle cells. IGFs promote either muscle cell differentiation or division, depending on oxygen availability.
Research discovers changes in muscle cell structure affecting gene expression and actin protein mutations causing muscle damage. The study sheds light on the biochemical pathways leading to nemaline myopathy, a rare inherited muscle-wasting disease.
Researchers have developed a new nanoscale scanning technique that provides unprecedented insight into the surface of individual heart muscle cells in minute detail. The findings may lead to better-designed beta-blockers and improved therapeutic approaches for treating heart failure and abnormal heart rhythms.
A study published in Nature Structural & Molecular Biology reveals that a genetic mutation disrupts an array of metabolic pathways in muscle cells by affecting two key proteins. The loss of either protein accounts for most molecular abnormalities associated with the disease, while loss of both also seems to play an important role.
Researchers find that muscles with inefficient energy-burning mechanisms contribute to obesity, proposing a potential anti-obesity strategy involving muscle-targeted treatments. Regular activity or exercise may increase muscle calorie burn, aiding weight control.
Researchers have identified Notch signaling pathway activation in human angiomyolipomas and TSC2-deficient rat cells, suggesting that TSC proteins regulate Notch activity. This finding supports the idea that Notch dysregulation may underlie some of the distinctive clinical features of Tuberous Sclerosis Complex.
Scientists at EMBL identify Notch signalling pathway as critical component of heart muscle cell communication, leading to heart defects and cardiac malformations in Alagille syndrome. Re-activating Notch improves adult mouse heart function after heart attack, offering new therapeutic potential.
A new study demonstrates that muscle cells grown in the lab can restore an intestine's ability to squeeze shut properly. The technique may strengthen sphincters, which are bands of muscle separating intestinal sections, and treat conditions like gastric reflux and fecal incontinence.
Researchers found that mice deficient in a gene required for autophagy develop muscle atrophy and weakening, resembling certain diseases. Maintaining normal autophagy levels is crucial to clear away damaged cells and prevent muscle weakness with age.
Scientists have found that odor-detecting tools in the nose, specifically MOR23, aid muscle cells' repair process. The receptor regulates cell migration and adhesion to form long fibers, offering potential new treatments for muscular dystrophies.
Researchers aim to use human pluripotent stem cells to produce cardiac myocytes for transplantation into diseased hearts. The study could potentially treat 500,000 new cases of heart disease annually.
Researchers identified a critical crosstalk pathway between lung epithelial cells and airway smooth muscle cells, contributing to lung diseases like asthma and pulmonary hypertension. The study provides potential new therapeutic targets for treating these conditions.
Researchers identified miR-143 and miR-145 as key regulators of VSMC contractility and blood pressure. The study found that mice lacking these microRNAs had reduced contractile VSMCs and increased tissue matrix-producing cells, leading to signs of blood vessel disease.
Researchers at the University of Arizona's Sarver Heart Center have developed a delivery system to introduce living, healthy heart muscle cells into damaged areas of the heart. The new approach uses a patch made from microscopically thin fibers that serve as a scaffold for the cells to adhere to.
Tiny membrane-bound compartments called vesicles rely on axon tension to dump neurotransmitters into the synapse. The researchers found that axons need tension to keep vesicles clustered near the synapse, essential for neuronal signaling. Further research is needed to understand the exact mechanism behind this process.
Researchers at UT Southwestern Medical Center will conduct basic science research projects to study the development and mechanisms of generating new cardiac muscle cells. The goal is to develop new therapeutics based on small molecules and microRNAs that will overcome barriers to heart regeneration.
Researchers have discovered that two microRNAs, miR-143 and miR-145, control the differentiation and growth of vascular smooth muscle cells. These findings suggest that targeting these microRNAs may be a potential treatment for diseases such as atherosclerosis and Alzheimer's disease.
Researchers at Gladstone Institute discovered a key switch, microRNA-145 (miR-145), to turn stem cells into muscle cells that reside in blood vessel walls. This finding suggests restoring miR-145 activity could prevent artery narrowing and vessel disease.
Guided fat precursor cells lead to wider nerves and less muscle atrophy in injured peripheral nerves of laboratory rats. The study demonstrates the potential benefit of adult precursor cells, such as those from adipose tissue, for nerve repair and functional recovery.
Researchers at King's College London discovered a key element in the development of chronic asthma, linking airway remodelling to muscle cell changes. The study found that reducing SERCA2 levels in airway muscle cells may lead to effective new treatments for severe asthma.
Bisphenol A (BPA) exposure may be associated with abnormal activity in female rat and mouse hearts, potentially leading to improper heartbeat control. Researchers found estrogen receptors play a key role in this effect, which could have significant implications for women's heart health.
Researchers found that a heart muscle protein, ACTC, can compensate for a lack of skeletal muscle protein, ACTA1, in mice with myopathy. Mice with this compensation survived more than three months and showed improved endurance, locomotor performance, and muscle strength.
Researchers found skin cells can become muscle-like and vice versa by changing who they associate with, providing insight into genetic reprogramming. This discovery may lead to more efficient ways to create stem cells and treat diseases like diabetes.
Researchers successfully transform human skin cells into mouse muscle cells and vice versa, providing insight into cell specialization and potentially bypassing stem cells. This breakthrough may lead to novel treatments for diseases by directly generating necessary cells.
A study published in the Biophysical Journal has discovered a method to predict heart attacks by measuring electrical activity coupling between two types of heart muscle cells. This can help doctors and patients buy time before an attack occurs.
Researchers confirmed that transplanting autologous muscle-derived cells into the bladder improves symptoms and quality of life in patients with stress urinary incontinence. The treatment has few side effects and significantly improved symptoms, with 76.5% of patients reporting a reduction in stress leaks at 12 months.
Researchers at Caltech have discovered a tiny genetic mutation that prevents nicotine from binding to muscle cells' acetylcholine receptors. This subtle difference explains why nicotine is virtually powerless in muscle cells despite being highly addictive in the brain.
A CU-Boulder research team has identified a type of skeletal muscle stem cell that contributes to the repair of damaged muscles in mice. The newly identified stem cells, dubbed satellite-SP cells, renew the satellite cell population after injection into injured muscle cells, contributing to recovery of muscle tissue.
Engineers at Purdue and Stanford universities have developed a new 'stretchable cell culture platform' to study the effects of mechanical stresses on cardiac muscle cells, neurons, and other cells. The device allows for electric stimulation or monitoring while applying stress, enabling researchers to test various cell types.
Researchers found that ankyrin-B protein plays a vital role in stabilizing microtubules and anchoring dystrophin to the muscle membrane, preventing cellular damage and death. The study provides new insights into the underlying mechanisms of muscular dystrophy.
Research reveals that mutations in the LMNA gene disrupt neuromuscular junction organization, leading to muscle fiber innervation disruption. This study provides insight into the molecular mechanisms underlying Emery-Dreifuss muscular dystrophy.
A study by Ohio State University researchers found that the molecule miR-29 is essential for muscle repair and maturation, but its absence is linked to rhabdomyosarcoma cancer. Raising miR-29 levels in cancer cells slowed tumor growth and induced maturity.
Researchers have identified a single gene, G9a, controlling cell flexibility in embryos and potential for medical cell replacement therapy. This discovery sheds light on the process of cell differentiation and could pave the way for new approaches to reprogram cells in a controlled manner.
Researchers have developed a mouse model of neonatal diabetes that replicates human disease, providing new insight into the condition. Additionally, studies have identified a link between endothelial dysfunction and altered metabolic responses, particularly in relation to high-fat diets and glucose regulation.
Researchers have effectively repaired damaged heart muscle using a novel population of stem cells derived from human skeletal muscle tissue. The transplanted myoendothelial cells improved heart function and reduced scar tissue, showing promise for regenerative medicine therapies.
Researchers discovered that adding sarcospan to muscle cells improves protection against Duchenne muscular dystrophy, a condition caused by faulty anchoring of the dystrophin protein. Sarcospan coaxes utrophin, a dystrophin relative, to spread out on the muscle membrane, providing additional protection.
Agrin and MuSK don't directly communicate, but LRP4 serves as a bridge to initiate critical internal cell talk. This finding sheds light on the agrin-MuSK signaling pathway's role in muscular dystrophy.
Researchers found that a heat shock protein, Hsp90β, helps stabilize rapsyn, an unstable protein responsible for anchoring receptors to catch messages from neurons. This discovery could lead to new treatments for muscular dystrophies and neurological disorders.