Articles tagged with Heart Muscle
Columbia University engineers develop a novel approach to growing mature human heart muscle from blood-derived stem cells, achieving critical hallmarks of adult human heart function in just four weeks. The technique involves applying physical conditioning and electromechanical stimulation to drive rapid maturation of the tissue.
A team of researchers at Michigan Technological University has created 3D substrates that mimic the natural heart environment, enabling cardiomyocytes to mature more quickly and have improved functionality. This breakthrough could lead to more effective treatment options for individuals with heart injuries.
A UTSW study found that inhibiting glucagon action has potent anti-diabetic effects, reducing negative fat tissue impacts and improving cardiac function. The research may advance understanding of diabetes drugs' benefits for heart health.
Researchers have mapped detailed molecular events underlying the transformation of ordinary fibroblast cells into therapeutic cardiac muscle cells. The study reveals key changes in protein levels, including a sharp rise in Agrin, which promotes repair processes and inhibits organ size regulation.
Researchers have identified a crucial mechanism in the regulation of titin protein, a key player in skeletal muscle and heart function. The study found that disulfide bonds play a significant role in determining titin's elastic properties, and their formation can cause major changes in the protein's elasticity.
Researchers created human cardiac-muscle patches that significantly improved recovery from heart attack injury in large animals. The patches also reduced infarct size, wall stress, and apoptosis, while preventing arrhythmia.
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 new study on mice sheds light on the role of protein modification in heart failure, suggesting new strategies for personalizing treatment by examining phosphorylation. Researchers found that abnormal addition of phosphate to a specific heart muscle protein may damage the heart's pumping ability.
Researchers at Baylor College of Medicine discovered that silencing the Hippo signaling pathway can reverse severe heart failure in an animal model. The study found that inhibiting this pathway induces heart muscle cell proliferation and reduces fibrosis, leading to improved heart function.
Researchers are developing living patches that mimic heart muscle cells, blood vessels and optical circuitry to create implantable heart tissue. The goal is to produce a true-to-life 'heart on a chip' to aid the pharmaceutical industry in developing better treatments for arrhythmia.
A new gene therapy has been found to be safe and effective in treating patients with coronary artery disease, enhancing circulation in the heart muscle. The biological bypass method involves injecting a natural human growth factor into the heart muscle to promote vascular growth.
Researchers identified a genetic variation underlying heart muscle regeneration in adult mammals. The study found that some individuals can naturally recover from a wounded heart due to higher percentages of regenerative cells, and that modulating the activity of a specific gene may enhance regeneration.
Researchers at Worcester Polytechnic Institute are developing a patch using biopolymer microthreads seeded with genetically engineered cardiac cells to improve heart function after a heart attack. The goal is to create a composite patch that can restore contractile function and provide additional strength and contractile force.
A new study found that intensive lowering of blood pressure reduced left ventricular hypertrophy (LVH) and prevented cardiovascular events. Lowering systolic blood pressure to less than120 mmHg improved heart muscle, but did not correlate with fewer incidents.
Washington State University researchers are studying mutations in three proteins that cause cardiomyopathy, a genetic heart condition affecting 1 in 500 people worldwide. The four-year project aims to improve diagnostics and develop new treatments for hereditary heart conditions.
A study published in JAMA found that patients undergoing noncardiac surgery with high-sensitivity troponin T levels after surgery were at higher risk of death within 30 days. The study analyzed data from over 21,800 participants and showed a significant association between elevated biomarkers and increased mortality.
A recent study has discovered that macrophages are essential for the normal functioning of the heart, helping conduct electric signals that coordinate heartbeat. The findings suggest that changes in macrophage numbers or properties may contribute to heart rhythm abnormalities.
Research by TUM found that low zinc levels can affect the heart's ability to deal with oxidative stress, leading to increased risk of heart disease. Zinc deficiency was also linked to upregulation of genes responsible for programmed cell death.
A team of scientists has identified a two-part system protecting the heart muscle's power grid from disease-related damage. The mitochondrial circuits in the heart are arranged in parallel rows, forming several smaller subnetworks that limit the spread of electrical dysfunction.
Researchers identify that cardiac muscle cells both destroy and create new mitochondria in response to ischemia/reperfusion injury, which can cause long-term effects or fatal heart failure. This discovery may lead to the development of new treatments to speed up healing from open-heart surgery.
Scientists at King's College London have developed a new blood test that detects damaged heart muscle caused by a heart attack more sensitively than current tests. This could lead to faster diagnosis and treatment of patients, while reducing unnecessary hospital admissions.
Researchers have grown engineered heart tissue using a 3-D printer, improving heart function and decreasing dead tissue after a heart attack. The novel technique holds promise for the clinical use of 3-D-printing technology in preventing heart failure after a heart attack.
Researchers developed an implantable soft-robotic device that gives the heart gentle squeezes, improving blood flow and reducing risk of infection. The device successfully restored normal blood flow in living pigs and could be tailored for individual patient needs with further investigation.
Researchers identified a genetic variant in MYBPC3 that predisposes South Asians to hypertrophic cardiomyopathy, an enlarged heart condition. Early screening of this variant can help reduce the incidence of sudden cardiac death in this population.
Researchers have developed a flexible, disposable sensor for monitoring proteins in the blood released from damaged heart muscle cells after a heart attack. The sensor uses nanostructures to detect low concentrations of troponins with high accuracy, enabling quick diagnosis and treatment at home.
Researchers discovered that inhibiting ANGPTL2 production can benefit both mice and human cardiac muscle cells with therapeutic effects in reducing heart failure progression. Moderate exercise previously found to reduce ANGPLT2 levels can now be replicated through gene therapy.
A team of University of Houston researchers has identified novel regulators of heart formation, including microRNAs, which can convert human fibroblasts into heart muscles. These findings hold promise for treating human heart attack and subsequent heart failure within the next five to 10 years.
Researchers found that circadian rhythms influence the influx of immune cells into damaged tissue, worsening heart attack outcomes. The study showed that neutrophil recruitment is correlated with CXCR2 expression and peaking in early morning hours, leading to increased inflammation and scar formation.
Researchers from Emory University School of Medicine have discovered that chymase inhibitors could extend cell survival after a heart attack. The study found that suppressing chymase activity can prevent late death of heart muscle cells, which occurs several days after blood flow is restored.
Researchers found that GSK3β inhibition improves cardiac function and reduces fibrosis and inflammation in murine models of arrhythmogenic cardiomyopathy. The study suggests GSK3β inhibition has potential as a therapeutic strategy for treating ACM.
Researchers discovered that microtubules interact with the heart's contractile machinery to provide mechanical resistance during contraction. Increasing detyrosination leads to increased myocyte stiffness and impeded contraction, while suppressing it enables the sarcomere to shorten more easily.
A new study has made significant progress toward a novel approach to convert scar tissue into healthy heart muscle, which could improve the quality of life for people with heart failure. By removing a barrier to conversion, researchers were able to significantly increase the yield of muscle-like cells.
A new study has discovered a type of noncoding RNA called Chast that drives heart failure in mice and may promote cardiac hypertrophy. The researchers found that targeting this lncRNA with an antisense oligonucleotide could prevent and treat cardiac hypertrophy, improving heart function.
Researchers reconstructed 3D images of intercalated discs, protein structures that connect heart muscle cells, and found clusters of proteins that work together to pass on electrical signals and pumping force. The discovery may lead to a simple blood test to detect life-threatening arrhythmias.
Researchers have successfully generated human cardiac muscle cells from stem cells using a 'Matrigel mattress', addressing a problem with contractile properties. The new method allows for high-throughput screens to find novel therapies for heart diseases, including hypertrophic cardiomyopathy.
Researchers at UT Southwestern Medical Center identified a previously unrecognized small protein, DWORF, in human heart cells that plays a key role in heart muscle contraction. The protein stimulates calcium-ion pumps to increase forceful pumping.
Scientists found that brief exposure to 'asynchrony' using a pacemaker can reverse cellular damage, fix damaged motor proteins in the heart muscle, and boost the heart's response to hormones like adrenaline. The therapy uses alternating electrical shocks to push the heart into normal synchronization for part of each day.
A study by Charité researchers has identified a specific protein and its splice variant as crucial in the development of cardiac hypertrophy. Initial activation of this protein leads to an increase in production of proteins associated with early cardiac development, causing the abnormal thickening of heart muscle.
A new study from Karolinska Institutet shows that the mouse heart generates a substantial number of muscle cells early in life, as does the human heart. After the neonatal period, the generation of new heart muscle cells stops and the heart growth mainly occurs by size increase of muscle cells.
A study of nearly 3,000 adults found significant differences in how male and female hearts change over time. The research suggests that men's and women's hearts may develop age-related heart failure for different reasons, highlighting the need for gender-tailored treatments.
Scientists at the University of Pennsylvania have identified a stem-like progenitor cell, called cardiomyoblast, that produces only heart muscle cells. This discovery is expected to accelerate research into cardiac therapies and potentially lead to new treatments for heart damage.
Researchers at UT Southwestern Medical Center identified a cell type that generates new heart muscle cells, which can divide and replenish damaged heart tissue. The discovery uses a new cell-tracing technique that may prove useful for regenerating diseased hearts and has implications for cellular turnover in other organs.
Researchers found that vinculin levels increase with age, altering the shape and performance of cardiac muscle cells, leading to a healthy adaptive change. The findings suggest that vinculin could be an important therapeutic target to slow down the decline of heart muscle vitality.
Researchers discover fructose's role in heart failure, finding it efficiently converts to fat and stimulates glycolysis. Fructose also activates HIF, leading to increased KHK-C production and a vicious cycle of growth and damage.
A new study published in Cell found that human heart muscle cells are primarily formed during childhood, with only 40% replaced throughout a person's life. This discovery suggests it may be possible to stimulate the rebuilding of lost heart tissue through therapeutic strategies.
Researchers found that oxidation in cardiac cells disrupts PKG's ability to shield the heart from stress. Oxidation-resistant forms of PKG, however, allow for better protection against disease.
Researchers found that honokiol reduces excess growth of cardiac muscle cells, decreases ventricular wall thickness, and protects heart muscle cells from oxidative stress. Honokiol activates SIRT3, a protective protein associated with delayed aging, stress resistance, and metabolic regulation.
Scientists have identified PDE-9 as the long-sought culprit in heart failure by analyzing lab animals and human heart cells. The enzyme interferes with the body's natural 'braking' system, leading to progressive weakening and stiffening of the heart muscle.
A study published in Cell Reports identified RBFox2 as a critical protein in the progression from weakened heart muscle to heart failure. The researchers found that reduced RBFox2 expression coincides with weakening of the heart muscle, suggesting a causal role in heart failure.
A new theoretical model proposes that heart muscle cells don't necessarily beat as a single entity, but rather as a bundle of contractile units. The alignment of these bundles is predicted to depend on the elasticity of the extracellular matrix and can affect the beating strength of the cell.
A Johns Hopkins study finds that protein BDNF maintains heart muscle vitality and may link depression to heart disease. The research suggests a possible biochemical explanation for the relationship between mental and physical well-being.
Researchers have found that post-heart-attack arrhythmias are triggered by a power grid-like failure inside cardiac cells, disrupting mitochondria and causing chaotic cell-to-cell signaling. This disruption can lead to life-threatening arrhythmias like fibrillation, but pretreatment with certain medications may help prevent them.
Researchers at Hebrew University of Jerusalem found Erbin acts as a brake against excessive heart muscle growth. The protein's damage leads to decreased function and severe growth, which may be targeted for cardiac gene therapy in heart failure and breast cancer patients.
Scientists discovered a surge of heart muscle cell division in young mice, increasing cardiac muscle cells by 40% and suggesting thyroid hormone could aid in children's treatment, offering an alternative to focusing on stem cells.
Researchers successfully restored damaged heart muscles in monkeys using human embryonic stem cells, suggesting a promising approach for human treatment. The therapy regenerated 40% of the damaged heart tissue and improved cardiac function in some treated animals, but also raised concerns about arrhythmias.
Researchers have identified the RAF1 gene as a cause of childhood-onset dilated cardiomyopathy, a progressive and potentially fatal heart condition. The study found that patients with this genetic variant showed increased activity of the protein mTOR, which can be inhibited with FDA-approved drugs.
A new human trial demonstrates the effectiveness of injecting bone marrow-derived stem cells into the heart muscle to improve heart function in patients with severe ischemic heart disease. The treatment improved heart pump function by 8.2 milliliters, compared to an increase of 6 milliliters in the placebo group.
A new blood test measures a protein called cardiac myosin binding protein-C (cMyBP-C) to detect heart attacks more quickly. cMyBP-C is released to the bloodstream within just 15 minutes of cardiac damage, rising to significant levels in three hours.
Researchers at the University of Missouri have successfully treated laboratory mice with a genetic heart defect using a new compound. The study found that the compound reduced the thickness of the mice's heart muscles and improved their cardiac functioning, offering potential hope for treating hypertrophic cardiomyopathy.
Researchers at Vanderbilt University have discovered that mechanical forces generated by the rhythmic expansion and contraction of cardiac muscle cells play an active role in the initial stage of heart valve formation. This study provides a new perspective on the process, shedding light on how to create artificial heart valves.