Researchers at Sanford Burnham Prebys discovered that blocking an energy transfer enzyme shifts mammalian hearts into a regenerative state, promoting regeneration and improving recovery after a heart attack. By modulating heart cell metabolism, scientists can potentially awaken the heart's dormant regenerative abilities.
Researchers from The University of Osaka found that treatment with five mRNAs effectively promoted cardiac repair and extended survival in mice with heart failure. The study showed that simultaneous administration of five therapeutic mRNAs reduced heart tissue damage and improved heart function.
A new trial found that using a microaxial flow pump before and during cardiac stenting procedures for high-risk heart attack patients with severe heart attacks did not reduce heart damage. The study, published in the Journal of the American College of Cardiology, also showed increased bleeding complications.
The study found that tunneling nanotube-like structures connect cells in the heart, enabling long-distance intercellular communication essential for heart formation. Disruption of these structures resulted in impaired ventricular wall morphogenesis and defective myocardial growth.
Researchers at Hokkaido University developed a technique to promote cardiac regeneration by activating mitochondrial function in transplanted cells. The study found that activated mitochondria improved cardiac function and suppressed myocardial fibrosis, suggesting a new approach for treating severe heart failure.
The Texas Heart Institute and The University of Texas at Austin receive a four-year, $2.37 million NIH grant to develop injectable hydrogel electrodes for preventing and managing ventricular arrhythmias. Researchers have already demonstrated the feasibility of pacing the heart using the hydrogel in a porcine model.
Scientists have discovered the origin of congenital coronary fistulae, a condition where abnormal connections form between blood vessels and heart chambers. This study may help improve early diagnosis and treatment of this condition, which affects up to 0.2% of patients undergoing medical examination.
Excessive trabeculation of the left ventricle does not coalesce into a compact myocardial wall, making 'LV non-compaction' an inaccurate term that should be discouraged. The review recommends using 'excessive trabeculation', which can be observed across various health and disease states.
Researchers discovered that myosin motor proteins must be activated before muscles can contract, potentially leading to breakthroughs in treating inherited cardiac conditions. This new understanding could lead to medical remedies for diseases like dilated cardiomyopathy and hypertrophic cardiomyopathy.
Researchers discover that oxytocin stimulates stem cells to migrate and develop into cardiomyocytes in zebrafish and human cell cultures. This could lead to the regeneration of damaged hearts after a heart attack. The study found that oxytocin also activates EpiPCs, which can replenish lost cardiomyocytes.
SourceFrontiers·JournalFrontiers in Cell and Developmental Biology·TypeExperimental study·DateSep 30, 2022
Researchers at RIKEN have discovered how marsupials' hearts can regenerate for several weeks after birth, allowing for potential treatment of human heart disease. They found that inhibiting a protein called AMPK extended the period of regeneration in both mice and opossums, with minimal scarring.
Researchers analyzed the gut microbiome of 1,241 middle-aged individuals and found that about half of the bacterial species were modified by drug treatment, while 75% of disturbances occurred in early stages of overweight and type 2 diabetes. The study suggests that an imbalanced gut microbiome may play a role in heart disease development
Cardiac fibroblasts can be directly reprogrammed to form beating heart muscle cells on soft surfaces that match the elasticity of native myocardium. This approach shows increased functional maturation and spontaneously beating iCMs, with implications for treating heart failure and myocardial infarction.
Researchers at the University of Helsinki have developed a tissue-engineered approach to stimulate myocardial regeneration in ischemic heart disease. The therapy uses autologous atrial appendage micrografts to improve functional recovery and preserve heart pumping function.
Scientists are developing new electrically active materials to repair damaged heart tissue. These materials can conduct electricity, stimulate heart muscle growth, and potentially overcome scar tissue that interferes with healthy heart function.
Researchers investigated Bax protein expression and myocardial changes in rabbits with acute left ventricle (LV) pressure overload. The study found that Bax protein expression decreased and morphological changes occurred, particularly on day 5 of the process.
Researchers studied cardiomyocyte autophagia in rabbits with acute focal ischemia. The study found that autophagy increases immediately after ischemia to protect cells, but decreases over time due to energy conservation. This mechanism helps prevent necrotic area expansion and cardiac death.
Scientists have discovered that hypoxia-inducible transcription factors (HIFs) establish metabolic boundaries between cardiomyocytes to regulate maturation and contraction of the muscle. This pathway challenges previous models on heart metabolism, playing a critical role in correct formation of ventricles.
A new long-acting cardioplegia solution has been shown to reduce cardiopulmonary bypass times and aortic cross-clamp durations, leading to faster recovery times and shorter ICU stays. The study found improved postoperative cardiac function and reduced morbidity in pediatric patients undergoing heart surgery.
Researchers at Georg-August-Universität Göttingen used parthenogenic stem cells to create cardiomyocytes and engineered heart muscle with normal properties. This breakthrough demonstrates the potential of parthenogenic stem cells for tissue engineering and could lead to new cell replacement therapies.
Research at Thomas Jefferson University found that inhibiting GRK2 reduces acute ischemia injury to the myocardium, protecting cardiac myocytes from damage. The absence of GRK2 activity leads to improved recovery from acute cardiac damage.
Researchers aim to determine if metabolic changes in 'hibernating' heart cells limit their ability to recover after revascularization. The grant builds on previous work using a novel pig model with hibernating myocardium.
Researchers at UB aim to improve heart function in hibernating myocardium using bone marrow mesenchymal stem cells. The study will investigate the effects of aging on MSC potency and develop optimized therapeutics for managing chronic coronary artery disease.