Articles tagged with Heart Muscle
Scientists have identified over 100 phosphorylation sites with regulatory potential on RNA-binding proteins, including RBM20, which plays a crucial role in titin synthesis and heart muscle diseases. These findings provide insight into the post-transcriptional regulation of gene expression.
Researchers have discovered that vesicles from human heart cells can repair damaged tissue and prevent lethal heart rhythm disorders. The treatment, using cardiosphere-derived cells (CDCs) and their secreted exosomes, showed improved heart rhythms and reduced scarring in animal models.
A new international study confirms the low risk of myopericarditis following COVID-19 vaccination, with a rate of 18 cases per million doses. The study found no statistically significant difference between the incidence of myopericarditis after COVID-19 vaccination and other vaccinations.
Researchers at Mount Sinai have developed a reproducible method to advance the maturation of human pluripotent stem cell-derived cardiomyocytes, which support heart muscle contraction. The new protocol enables efficient energy generation from both carbohydrates and fatty acids, improving disease modeling and regenerative therapies.
A recent clinical trial has shown that sodium thiosulfate does not reduce injury to damaged areas of heart muscle following a heart attack. Despite promising results in animal studies, the trial did not meet its primary endpoint or show significant differences in secondary endpoints.
Researchers found significant and sustained improvements in left ventricular outflow tract gradients, health status, symptoms, and exercise capacity among patients taking mavacamten. The drug appears to be safe and well-tolerated long-term with no new adverse events reported.
A new clinical trial found that the drug mavacamten alleviates shortness of breath in patients with obstructive hypertrophic cardiomyopathy. The treatment also improves symptoms and heart failure biomarkers.
A phase 3 study found that mavacamten significantly improved symptoms, quality of life, and key heart markers in patients with obstructive HCM. Only 17.9% of those on mavacamten were still eligible for surgical intervention after 16 weeks, compared to 76.8% on placebo.
A preclinical study suggests that SARS-CoV-2 infection can cause ferroptosis in pacemaker cells, leading to cardiac arrhythmias. Researchers used animal models and human stem cell-derived pacemaker cells to demonstrate the virus's impact on these cells.
Researchers developed a novel approach to diagnose, monitor, and predict the course of myocarditis using CMR parameters and AI. The goal is to provide personalized counseling for athletes and optimize treatment options.
Dr. Zhiqiang Lin has been awarded a $3.2 million NIH grant to investigate the roles of YAP and IRF2BP2 in the cardiac innate immune response, with the goal of reducing cardiac inflammation and promoting heart recovery after a heart attack.
Robert Gourdie, a cardiovascular scientist at the Fralin Biomedical Research Institute at VTC, has been awarded an R35 grant from the National Heart, Lung, and Blood Institute. This seven-year, $6.4 million grant enables him to pursue research on intercellular communication and its applications in treating various medical challenges.
Researchers have discovered that bioprosthetic heart valve patients develop an immune response against foreign sugars in the valves, leading to calcification and deterioration. By genetically engineering these sugars out of the valves, durability can be increased, offering a potential solution for patients.
A small study found statistically significant improvements in various symptoms, including fatigue and chest discomfort, after EECP therapy in long COVID patients. Researchers believe this is the most plausible explanation for the benefits derived from EECP and its link to long COVID.
Biomedical engineers at Duke University have developed a gene therapy that helps heart muscle cells electrically activate in live mice. The approach features engineered bacterial genes that code for sodium ion channels, which could lead to therapies to treat electrical heart diseases and disorders.
A study by Indiana University School of Medicine researchers suggests that reperfusion therapy may not be as effective in halting muscle damage during heart attacks as previously thought. The team's findings indicate that internal bleeding within the heart muscle can continue to cause damage even after the blocked coronary artery is op...
Scientists have created a new tool that monitors the electrical activity inside individual heart cells using tiny 'pop-up' sensors. The device directly measures signal movement and speed within single heart cells and between multiple cells, offering potential breakthroughs in diagnosing arrhythmia and cardiac fibrosis.
A recent study published by Queen Mary University of London has found that certain risk factors for heart disease are linked to changes in the structure and appearance of the heart. The research analyzed images from over 30,000 people's heart MRI scans using a new imaging toolkit called radiomics.
Researchers from Göttingen University and Hannover Medical School have detected changes in heart muscle tissue of people who died from Covid-19. The study used innovative X-ray imaging to visualize the affected tissue in three dimensions, revealing a network of chaotic vessel formations.
Researchers found that up to one in five patients experience increased troponin levels after major surgery, indicating potential heart damage. These patients were also more likely to be anaemic before the operation.
Researchers at Johns Hopkins Medicine have discovered that manipulating certain nerve cells may trigger the formation of new heart muscle cells, restoring heart function after heart attacks. The study found that removing specific genes associated with circadian rhythms increased neonatal heart size and cardiomyocyte numbers by up to 10%.
Researchers at the Max Delbrück Center have developed a therapeutic agent to improve treatment of heart failure with preserved ejection fraction. The new approach targets alternative splicing in cardiac disease, using antisense oligonucleotides to stabilize sensitive molecules and trigger desired response.
Recent clinical trials showed promising results with cardiosphere-derived cells, improving heart parameters in patients with Duchenne muscular dystrophy. Researchers investigate using cell-derived products like exosomes to boost endogenous repair pathways, while aiming to reverse cardiomyocytes' proliferation limitations.
Researchers at Penn Medicine have made a major advance in understanding dilated cardiomyopathy (DCM), a common and fatal heart disorder. The largest single cause of DCM involves the mutation of the gene that encodes titin, leading to abnormalities in heart muscle cells.
A new guideline from the American Heart Association and American College of Cardiology recommends using standardized risk assessments and clinical pathways to evaluate chest pain. Most adults presenting with chest pain will have a non-cardiac reason, while only a small percentage will have an acute coronary syndrome.
Researchers developed a new system to measure and stimulate the entire ventricular surface of mouse hearts, allowing for simultaneous optical and electrical tracking of heart activity. The POEMS system provides accurate measurements of action potential propagation with minimal differences between modalities.
Researchers found that radiation therapy triggers heart muscle cells to express different genes and increase sodium ion channels, reducing arrhythmias. The treatment also continued to show benefits for at least two years in surviving patients.
The study found that the Wntless (Wls) gene plays a critical role in heart regeneration in mice by facilitating signal molecule secretion from cardiomyocytes to cardiac fibroblasts. This promotes heart functional recovery by suppressing CF activation and reducing scar formation.
Researchers found that using the 'no-touch' technique to remove leg veins during coronary artery bypass surgery resulted in fewer blocked grafts and a lower incidence of recurrent chest pain. However, the technique was associated with more wound complications, particularly in female patients with type 2 diabetes or hypertension.
A preclinical study found that age-related decline in two sirtuin enzymes alters mitochondrial dynamics, weakening cardiac contractions in response to ischemia-reperfusion injury. Boosting SIRT1/SIRT3 levels may help protect against such injuries, potentially reducing heart attack complications and deaths.
A new study found that 44% of micro-arteries from patients had abnormal myogenic tone, associated with excessive caldesmon presence and poor cell alignment. This abnormality affects blood supply within the heart and other organs, impacting quality of life and life expectancy.
Researchers have created a dynamic model that accurately recreates hemodynamic loads on engineered heart muscle tissues, providing unprecedented insights into how genetics and mechanical forces contribute to heart muscle function. This breakthrough model allows for the study of various heart diseases with genetic mutations, development...
Researchers discovered a three-step molecular process behind cardiac atrophy, which can lead to fatal heart failure. The study suggests potential new ways to prevent or treat the problem by eliminating or reducing the activity of specific genes.
New study reveals that the location of beta1 and beta2 receptors on heart muscle cells determines their functional effects, with beta1 receptors triggering persistent changes and gene activation. This knowledge could lead to more targeted therapies for chronic heart failure.
Early-phase trial found pirfenidone significantly reduced a marker of heart muscle scarring compared to placebo in patients with preserved ejection fraction. The study suggests that fibrosis is an effective treatment target and could lead to personalized approaches to prevent or reverse scarring.
Scientists have discovered a critical new gene, Klf1, that plays a vital role in healing damaged hearts. The gene allows heart muscle cells to divide and multiply after injury, potentially leading to complete regeneration and healing of damaged tissue.
Scientists have solved a fundamental mystery about how the heart works, revealing a new avenue for heart disease research. The discovery could lead to the development of new treatments for heart diseases, which are the leading cause of death worldwide.
Researchers at Wayne State University aim to address impaired relaxation of heart muscles through novel biomechanical tests and imaging techniques. The project, funded by the National Heart, Lung, and Blood Institute, will investigate how mechanical properties of the heart relate to models of heart failure.
Exercise reduces severity of heart failure, improves heart function, and increases work capacity in rats with heart disease. High-intensity training reverses dysfunctional calcium handling and improves electrical signals in the heart.
A team of researchers has discovered the atomic-level mechanism that governs the length of heart muscle protein filaments, a critical component in maintaining healthy heart function. The study provides new insights into genetic mutations that cause devastating hereditary heart conditions.
A study of 22 COVID-19 patient autopsies found a unique pattern of cell death in scattered heart muscle cells, challenging traditional myocarditis theories. The researchers propose several theories to explain the cardiac injury and suggest further investigation for potential treatment interventions.
Researchers discovered that zebrafish heart muscle cells switch from fatty acids to sugars for energy, enabling regeneration. This metabolic shift is crucial for heart regeneration and may hold potential for human heart regeneration after a heart attack.
A study published in Circulation reveals that an imbalance in the ratio of active and inactive myosin protein disrupts heart muscle contraction and relaxation, leading to hypertrophic cardiomyopathy. Treatment with a small-molecule drug restores proper contraction and energy consumption in human and rodent heart cells.
CryoEM technique reveals structural changes in cardiac muscle thin filaments that regulate heartbeat function. The study provides a molecular basis for novel drug design to treat diseases such as cardiomyopathy.
Researchers at Baylor College of Medicine discovered that inactivating the Hippo pathway in cardiac fibroblasts promotes cardiac fibrosis and adversely affects cardiac function. This finding highlights the need for specific targeting of the Hippo pathway in cardiac muscle cells for safe and effective heart failure therapy.
Researchers at Medical College of Georgia have identified a chemical that can improve communication between the body's smallest blood vessels and larger vessels, which is crucial for delivering oxygen to the heart muscle. By blocking an enzyme that inhibits this chemical, they found that it can reduce diastolic heart failure symptoms.
Autopsies reveal that meth users have increased deposits of collagen in the heart muscle, leading to irreversible damage and an enlarged heart. The study suggests that monitoring heart function is crucial for early detection and prevention of further deterioration.
Researchers identified hundreds of DNA regions associated with differences in gene expression between individuals, revealing potential links to complex diseases. The study's novel approach using induced pluripotent stem cells and daily RNA sampling sheds light on the dynamic nature of gene expression during cellular development.
Researchers at Imperial College London have developed lab-grown heart patches that are safe for human trials after clearing important hurdles. These patches contain up to 50 million human stem cells programmed to turn into working heart muscle, potentially curing debilitating heart failure.
A study found that metformin reduces left ventricular hypertrophy (LVH) in prediabetic and pre-existing heart disease patients, leading to lower cardiovascular risks. The MET-REMODEL Trial showed significant benefits of metformin on LVH, blood pressure, oxidative stress, and body weight.
Researchers discovered a genetic variant in troponin I that disrupts calcium-binding affinity in thin muscle filaments, leading to arrhythmias in human cardiac cells. This finding may contribute to SUDI by triggering sudden cardiac arrest.
A study from the Intermountain Healthcare Heart Institute has identified eight new gene mutations that may cause or contribute to idiopathic dilated cardiomyopathy, a form of heart disease not caused by known external influences. The researchers found that at least 40% of patients have an underlying genetic cause for the disease.
Researchers at Harvard Medical School have identified a faulty molecular brake that interferes with the heart muscle's ability to contract and relax. The study found that a mutation in the MyBPC3 gene leads to an overactive motor that propels abnormal muscle contractions, causing the heart to beat too much and relax poorly.
Researchers at the Hubrecht Institute found that adult hearts do not have stem cells that can regenerate lost heart muscle after a heart attack. Instead, connective tissue cells produce scar tissue to replace the lost cardiac muscle, which helps maintain heart integrity.
Researchers at the University of Arizona have identified multiple subpopulations of cardiomyocytes expressing specific transcription factors, which could lead to better repair of heart muscle injuries. The study uses a systems-based approach encompassing single-cell transcriptomics, single-cell proteomics and CRISPR gene-editing.
Loyola Medicine is testing a new catheter ablation system called Durablate that can destroy troublesome heart tissue not accessible to standard techniques. This approach may improve treatment outcomes for patients with ventricular tachycardia.
Researchers have identified serum response factor (SRF) as a critical regulator of cardiomyocyte maturation. SRF plays a key role in organizing contractile structures and regulating gene expression, but its level affects cell maturity. The study provides new insights into heart muscle development and regeneration.
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.
Researchers discovered a genetic mutation in troponin T that disrupts the heart's ability to increase pumping force when needed. This limits the heart's capacity to pump additional blood around the body, potentially leading to severe consequences for individuals with hypertrophic cardiomyopathy.