Articles tagged with Heart Muscle
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.
Researchers at the University of Michigan have successfully reprogrammed scar tissue cells to form colonies of beating heart cells. The discovery could pave the way for regenerating damaged heart tissue after a heart attack.
Researchers have identified Sca1 stem cells as the key players in the regeneration of heart muscle cells in mammals. These stem cells increase their activity in response to heart damage, leading to the formation of new heart muscle cells.
Researchers found that strenuous exercise like running a marathon causes temporary changes in the heart muscle, particularly in less fit distance runners. These changes are reversible but highlight the need for proper preparation before marathons to minimize potential damage.
New research reveals that blocking cell death proteins can prevent abnormal heart muscle thickening in animal models. This breakthrough could lead to new strategies for treating certain forms of heart disease, including hypertension and genetic conditions.
Researchers have identified a link between mitochondrial development and the origins of some congenital heart defects. Mitochondria orchestrate events that determine a cell's future, including whether it becomes heart muscle cells.
Cardiac muscle cells can be purified using molecular beacons, enabling their use in treating heart diseases. The technique has broad applications across regenerative medicine.
A biomedical research team at Worcester Polytechnic Institute will use a new microthread technology to deliver adult stem cells into damaged hearts, aiming to promote muscle regeneration and improve heart function. The five-year project aims to advance cell therapies for people suffering from heart disease.
Researchers have found that a drug already approved to treat multiple sclerosis may also slow and potentially reverse cardiac hypertrophy, a disorder that often leads to heart failure. By mimicking certain lipids in the body, FTY-720 significantly reduces heart mass and improves overall cardiac function.
Scientists at St. Jude Children's Research Hospital discovered that protein MCL1 is essential for normal cardiac function, complicating cancer drug development efforts. The study suggests that targeting MCL1 expression in target cells may be beneficial for treating heart muscle damage following heart attacks or other insults.
A longitudinal study found that people who carry excess weight over their lifetime have increased left ventricular mass and relative wall thickness, strong predictors of cardiovascular morbidity and mortality. The earlier someone becomes overweight, the greater the increase in heart muscle mass later in life.
Midwall fibrosis detected via MRI is associated with higher mortality rates in patients with nonischemic dilated cardiomyopathy. Patients with midwall fibrosis are at an increased risk of sudden cardiac death and cardiovascular mortality.
Researchers at Yale University identified a molecular mechanism by which the growth of new blood vessels and heart muscle are coordinated. Nitric oxide triggers the destruction of RGS4, allowing for physiological changes associated with the relaxation of blood vessels, while promoting cardiac growth.
Researchers used X-rays to recreate a microscopic crime scene and caught the arrhythmia culprit in action. Gene mutations destabilize the calcium pathway, causing premature release and potentially deadly conditions.
A recent study found a link between certain antidepressants and long QT intervals, a marker for heart rhythm abnormalities. The research used electronic health records to track patients who had taken antidepressants or methadone, and discovered that some medications increased the risk of abnormal heart rhythms.
Scientists develop the first maturation-based disease model for arrhythmogenic right ventricular dysplasia/cardiomyopathy (ARVD/C) using patient skin cells. The model mimics adult-onset disease by inducing adult-like metabolism, revealing metabolic malfunction and abnormal protein activation as key drivers of the disease.
Researchers at Boston Children's Hospital found that young humans can generate new heart muscle cells, challenging the accepted wisdom on human heart growth. The study's findings offer a potential new approach to treating heart failure in children by stimulating cardiomyocyte proliferation.
Researchers in Ghent have identified a new mutation in the CTNNA3 gene associated with arrhythmogenic right ventricular cardiomyopathy (ARVC), a hereditary heart condition that can lead to sudden cardiac death. The discovery could improve ARVC screening by including the CTNNA3 gene in genetic tests.
The study identifies two surface markers Flt1 and Flt4 on cardiovascular progenitor cells, allowing scientists to isolate and mature these cells into functional heart muscle cells. This breakthrough could revolutionize the treatment of heart disease by replacing lost cardiomyocytes.
Researchers have developed a low-energy defibrillation scheme that significantly reduces the energy needed to re-establish a normal rhythm in the heart's main chambers. This novel electrotherapy could be less painful than existing implantable defibrillators and may even fall beneath the threshold at which patients begin to perceive pain.
A recent study published in The New England Journal of Medicine found that cardiac bypass surgery is superior to percutaneous coronary intervention (PCI) for adults with diabetes and multi-vessel coronary heart disease. After five years, the CABG group had fewer adverse events and better survival rates than the PCI group.
Researchers at NHCS have developed a novel human heart cell model of ARVC, allowing for safer study of genetic cardiovascular diseases and risk stratification. The model replicates key characteristics of the disease, including abnormal fatty changes and altered desmosomal proteins.
Researchers found that troponin I's phosphorylation levels are altered in patients with heart failure, leading to muscle dysfunction. The discovery paves the way for new diagnostic tools and therapies for heart failure, a condition affecting over 6 million adults in the US.
Researchers have made a major advance in efforts to regenerate damaged hearts by transplanting human cardiac muscle cells that electrically couple and beat in sync with the heart's own muscle. These grafts reduced the incidence of arrhythmias in a guinea pig model of myocardial infarction.
A $4.7 million study aims to investigate why people with diabetes suffer from unusually severe forms of heart disease. The researchers suspect that abnormal lipid metabolism is a key culprit, leading to inflammation and damage to heart cells.
Scientists at Joslin Diabetes Center have identified a new cause of cardiac damage after heart attacks in people with type 1 diabetes. A runaway autoimmune response triggered by alpha-myosin leads to chronic inflammation, cardiomyopathy, and heart failure. The study offers promising targets for future interventions to protect the heart.
Researchers at Imperial College London found that allowing heart muscle cells to rest can reverse structural changes caused by heart failure. This discovery could lead to new treatment strategies without the need for serious procedures like LVAD implants.
A new comparative effectiveness study found that older adults who underwent bypass surgery had better long-term survival rates than those who underwent a non-surgical procedure to improve blood flow to the heart muscle. After four years, the CABG group had a 21 percent lower mortality rate compared to the PCI group.
Researchers discovered that abciximab significantly decreased heart muscle damage in ST-segment-elevation myocardial infarction patients. Clot aspiration did not show similar benefits.
Researchers identified 72 mutations in the TTN gene that cause structural deformations in heart muscle fibers, leading to heart muscle disease. The study found that TTN gene mutation causes DCM, but rarely causes hypertrophic cardiomyopathy, and that outcomes for patients with DCM are similar regardless of gender.
Researchers identified a family of molecules that can stimulate stem cells to develop into beating heart muscle cells, paving the way for new therapies for cardiac regeneration and repair. The discoveries were made using a zebrafish model system and showed promise in enhancing the inherent regenerative capacities of the heart.
Researchers identify oncostatin M as a key player in the self-healing powers of the heart, allowing damaged heart muscle cells to reversion and produce new cells. This discovery holds promise for treating heart disease, but further research is needed to pinpoint the precise window of application.
A new study published in Neurology found that a person's stroke risk profile can also predict their risk of developing memory and thinking problems later in life. The researchers followed 23,752 people with an average age of 64 and found that those with higher stroke risk profiles were more likely to develop cognitive problems.
Researchers at Johns Hopkins Medicine found that a widely used pacemaker for heart failure works by raising regulator of G-protein-signaling proteins in the heart. This helps restore balance between two proteins, allowing the heart muscle to respond to hormones like adrenaline more effectively.
The first clinical studies of omecamtiv mecarbil suggest it could be a promising treatment for systolic heart failure, improving heart muscle contraction and pumping function. The drug has dose-dependent and concentration-dependent effects on cardiac function, increasing stroke volume, ejection fraction, and fractional shortening.
Researchers found that adult stem cells from the human nose can repair damaged brain tissue, while a cancer probe made of silica nanoparticles is effective at targeting tumors. Additionally, inhibiting a protein MRP4 could provide a new way to treat pulmonary hypertension.
Researchers found that a specific type of immune cell attacks the heart muscle because it fails to develop tolerance against a unique protein. This leads to inflammation and potentially fatal consequences, highlighting the need for targeted therapies. The study's findings have significant implications for treating autoimmune myocarditis.
Researchers at Mount Sinai School of Medicine found a direct correlation between elevated troponin and creatine phosphokinase levels and increased risk of death, even among those who initially recover well from CABG surgery.
A new study in mice suggests that exercise turns on a genetic program that leads the heart to grow as heart muscle cells divide. Researchers identified a key transcription factor involved in this process, which may have clinical implications for those with heart failure or other conditions.
Researchers found that functional cardiac stem cells can be isolated from aged and damaged hearts, with women producing more CSCs than men. The study suggests that these stem cells have the potential to regenerate heart muscle and vessel tissue, potentially treating heart failure.
A 44-year-old sailor received a groundbreaking treatment for severe myocarditis, which caused inflammation of his heart muscle and led to heart failure. He was implanted with two small ventricular assist devices, making him the first person in North America to receive this life-saving therapy.
A team of researchers at the University of Pennsylvania School Medicine discovered a three-way control mechanism for fetal heart cell proliferation. This finding could help cardiologists understand the natural repair process after heart attacks and develop new therapies to expand cardiac stem cells.
Bonn researchers have developed a method to trigger arrhythmia in mice using light stimulation, allowing them to study the condition with unprecedented precision. By selectively targeting specific areas of the heart muscle, scientists can induce ventricular fibrillation, a common cause of death after a heart attack.
A study by University of Iowa researchers found that structural defects in heart muscle cells occur before functional decline, suggesting a potential window for intervention. The team used imaging techniques to visualize changes in T-tubule networks, which were accompanied by reduced junctophilin-2 levels and compromised integrity.
Researchers have devised a three-ingredient molecular cocktail that transforms fibroblasts into beating heart cells, potentially solving the issue of cardiac muscle regeneration in heart disease. The cocktail, tested on mice, shows promise in producing new cardiac muscle cells more efficiently than induced pluripotent stem cells.
Researchers identify zebrafish heart cell population that regenerates cardiac muscle cells, challenging traditional view of stem cells in regeneration. Human hearts cannot replicate this process, but finding could provide insight into hibernating mammalian cardiomyocytes and potential regeneration strategies.
Smadar Cohen's groundbreaking research led to the development of an innovative cardiac scaffold that enhances mechanical strength and prevents enlargement of the left ventricle. The award recognizes her pioneering work in creating a resorbable liquid polymer, BL-1040, that promotes heart muscle recovery and repair.
A new pilot study led by UC and VA researchers is evaluating the functional significance of blockages in cardiac blood vessels. Using a formula derived from fluid mechanics principles, they aim to provide more accurate assessments of vessel blockages.