Researchers at CNIC discover clonal hematopoiesis as a new cause of atherosclerosis, while identifying the ancient medication colchicine as a potential treatment. Clonal hematopoiesis is linked to an increased risk of cardiovascular disease, with no influence on the progression of mutated blood cells.
A large-scale study published in JACC shows that promoting healthy habits in elementary school children can effectively reduce abdominal fat and obesity markers. The study found that early intervention, particularly during the first three years of school, was more effective than delayed interventions.
A CNIC team has developed iSuRe-HadCre, a novel genetic tool that enables precise and efficient gene modification in mouse models. This new technology overcomes limitations of existing methods, offering improved efficiency, precision, and applicability in biomedical research.
A Danish-Spanish collaboration is launching the REACT initiative to develop early detection and prevention methods for atherosclerosis. The project aims to identify new means to detect atherosclerosis at earlier stages and at a younger age, enabling precision treatment and prevention.
A CNIC study explores the mechanisms of supercomplex assembly and uncovers a major impact of mitochondrial assembly factors on cardiac regeneration. The researchers found that Cox7a1 plays a fundamental role in forming CIV dimers, which are crucial for correct mitochondrial function.
Researchers discovered that eliminating progerin from vascular smooth muscle cells prevents atherosclerosis and improves life expectancy in HGPSrev mice. This finding suggests a potential therapeutic strategy for treating progeria, an extremely rare genetic disease affecting 1 in every 20 million people.
A new Spanish study provides the first stratification of the risk of developing dilated cardiomyopathy among symptom-free genetic carriers. Researchers found that nearly 11% of genetic carriers developed the disease within a median follow-up period of 37 months.
The REACTIVA project aims to establish a new strategy for cardiac regeneration based on reactivating the heart's dormant endogenous mechanism. Researchers will investigate the role of diploid adult cardiomyocytes in cardiac regeneration and use this knowledge to induce their activation.
Scientists at CNIC have identified mechanisms by which anthracyclines damage the hearts of cancer patients, leading to cardiac injury. The study suggests that a protein-enriched diet may prevent muscle atrophy caused by anthracycline chemotherapy.
Researchers have discovered a direct link between the C122Y mutation in the Kir2.1 potassium channel and life-threatening arrhythmias in Andersen-Tawil syndrome, which affects fewer than 1 in a million people. The study highlights the importance of understanding the molecular mechanisms underlying cardiac arrhythmias.
Researchers discovered that reducing cholesterol levels in mice with advanced atherosclerosis leads to a decrease in the number of smooth muscle-derived cells causing plaque growth, while preserving stabilizing cell types. This finding opens up new opportunities for targeted therapies.
The study found that APOE4 carriers have elevated LDL cholesterol levels, increasing their risk of developing subclinical atherosclerosis. In contrast, APOE2 carriers have lower cholesterol and reduced atherosclerosis prevalence.
A study published in Science Advances identifies a mitochondrial protein called MCJ as the first therapeutic target to preserve cardiac function in pulmonary hypertension. Modulating MCJ levels can activate a signaling pathway essential for adaptation to low oxygen levels, protecting the heart.
Researchers at the Centro Nacional de Investigaciones Cardiovasculares discovered the molecular mechanisms behind proper heart valve formation and prevention of calcification. They found that Notch signaling pathway disruption causes both valve defects and calcification.
The Joint Action on Cardiovascular Diseases and Diabetes (JACARDI) aims to reduce the burden of cardiovascular diseases and diabetes in EU member states through 143 pilot projects. The project will test and offer solutions throughout the patient journey, focusing on prevention, early detection, treatment, care, and self-management.
Researchers at the CNIC in Madrid have discovered a connection between stress kinases and the development of ventricular fibrillation. The study found that activation of these enzymes alters the electrical properties of cardiomyocytes, triggering arrhythmias.
A new study reveals that younger people are more vulnerable to the effects of high blood cholesterol and hypertension, atherosclerosis can be reversed if risk factors are controlled early enough. The study suggests aggressive control of cardiovascular risk factors at younger ages.
Researchers at CNIC reveal the essential role of neuregulin-1 in transforming the delicate primordial heart structure into a powerful pumping organ. The study sheds light on the pathways of human heart formation and suggests new strategies for heart health and regenerative medicine.
A team of Spanish scientists discovered profound changes in dendritic cells during the immune response, which could lead to novel vaccines against bacterial and viral infections. The study found increased lipid peroxidation and MHC-I upregulation in post-synaptic dendritic cells, triggering efficient priming of CD8+ T cells.
A study published in Diabetes Care found that obesity, hypertension, and dyslipidemia alter cardiac energy production by interfering with metabolic substrate uptake. The research reveals early changes in apparently healthy middle-aged individuals, highlighting the importance of identifying mechanisms involved in heart disease onset.
A new CNIC study confirms that controlling traditional cardiovascular risk factors can prevent Alzheimer's disease and dementia. Maintaining a low cardiovascular risk is linked to preserved cerebral glucose metabolism, indicating better brain health.
A new diagnostic method assesses electrical and mechanical activity in the heart during atrial fibrillation, providing personalized assessment of atrial remodeling. This can help predict disease progression and guide treatment.
A new study reveals that biscuspid aortic valve is caused by mutations in the MINDBOMB1 gene, with significant implications for developing alternative treatments to surgery. The research combines genome sequencing and gene editing techniques to analyze the mechanisms of this congenital defect.
A new study by CNIC researchers reveals that low-grade systemic inflammation triggered by subclinical atherosclerosis accelerates epigenetic aging in otherwise healthy young individuals. The study found a strong association between atherosclerosis progression and accelerated biological age, with potential reversibility through lifestyl...
Researchers discovered that vascular toxicity linked to these drugs is unrelated to angiogenesis-related genes, but rather due to changes in vascular architecture. This new understanding will help select the most effective and safe way to modulate angiogenesis in ischemic tissues or cancer.
A study by CNIC researchers reveals that gamma-linolenic acid in breast milk binds to the retinoid X receptor protein, activating gene expression and influencing biological functions. This activation initiates genetic programs that equip mitochondria with the necessary enzymes and proteins to start consuming lipids as energy.
Researchers have developed a pharmacological treatment that improves cardiac function in patients with stiff-heart syndrome, a condition caused by amyloid protein deposition. The new drug reduces amyloid protein deposits and shows promise in reversing established disease symptoms.
A recent MRI study by the CNIC has established reference values for anatomical and functional parameters in adolescents' hearts, providing a crucial resource for clinical practice. The study involved 123 adolescents and aimed to fill the knowledge gap on 'normal' cardiac parameter values in this age group.
Macrophages adapt their metabolism according to the organ they reside in, reveals Spanish scientists. This discovery highlights a vulnerability of macrophages that contributes to chronic inflammatory diseases and could be exploited therapeutically for conditions like cardiovascular disease and type 2 diabetes.
Researchers found that p53 mutations in blood cells increase the risk of developing coronary heart disease and peripheral artery disease. The study provides solid evidence for the link between acquired p53 gene mutations and cardiovascular disease, suggesting a potential new risk factor.
The CNIC study reveals two distinct mechanisms by which cells detect and respond to forces of varying strength, one mediated by caveolae and the other by newly discovered dolines. This finding has significant implications for understanding pathological processes such as atherosclerosis and neurodegenerative diseases.
The study shows that RXR ensures hematopoietic stem cells remain youthful and fit, reducing the risk of developing myeloproliferative syndromes. The regulatory action of RXR on these cells is essential for maintaining a balanced production of blood cell types throughout life.
A new gene therapy approach has been developed to boost the expression of the beta-3 adrenergic receptor in heart cells, improving mitochondrial function and preventing or reversing heart failure in a mouse model of aortic stenosis. This could potentially provide new therapeutic options for patients with this condition.
Researchers found that the presence of one Mindbomb1 mutation does not always lead to non-compaction cardiomyopathy, but depends on genetic context provided by other gene mutations. The study identified modifier genes contributing to disease severity and diversity in affected individuals.
Researchers at CNIC have identified metoprolol as a neuroprotective agent after a stroke, greatly reducing cerebral inflammation and neuronal death. The study's findings suggest that metoprolol may also offer benefits in treating severe Covid-19.
A new software application predicts the likelihood that a case of dilated cardiomyopathy has a genetic mutation. The Madrid Genotype Score identifies patients most likely to have inherited the disease, facilitating genetic screening and tailored treatment adjustments.
A study by CNIC scientists has identified a key role for the MKK3/6–p38γ/δ signaling pathway in cardiac hypertrophy. Inhibition of p38α promotes an unexpected activation of the other branch of the pathway, consisting of the proteins MKK3, p38γ, and p38δ. This activation induces another key pathway in cardiac hypertrophy, the mTOR pathway.
A Spanish study combines genetic and imaging data to predict patient prognosis, identifying those at risk of malignant arrhythmias or severe complications. The findings open the way for personalized medicine in treating dilated cardiomyopathy.
A study published in the European Heart Journal found that making small behavioral changes can significantly reduce cardiovascular risk. Participants who received a lifestyle intervention showed improvements in physical activity, diet, and sedentary time, leading to decreased blood pressure and cholesterol levels.
Scientists at CNIC discovered a complex network between liver tissue connections that allows the liver to regulate body temperature. The secretion of IL-12 by liver-infiltrating macrophages blocks FGF21 production, reducing heat generation by brown fat in mice.
A CNIC team has created a dynamic 3D atlas of the formation of the heart during embryonic and fetal development, allowing for the identification of the first appearance of left–right asymmetry in the heart. This study provides important information on the development of congenital heart malformations.
Researchers have identified a new mechanism involving the oxidation of cysteines in titin protein that modulates cardiac stiffness and dynamics. This discovery sheds light on how the heart adapts to various situations and responds to oxidative balance disorders.
A study identifies new biomarkers that predict the presence of subclinical atherosclerosis, providing a non-invasive way to detect cardiovascular disease. The research team analyzed blood plasma samples and validated three proteins as biomarkers, improving the prediction of cardiovascular risk.
Researchers at CNIC discover that bone marrow activation is an early event in the development of atherosclerosis, leading to inflammation and plaque formation. The study identifies metabolic syndrome as a key trigger for this process.
A new 3D matrix ultrasound method has been developed to assess cardiovascular risk in healthy individuals, offering a reliable and accurate alternative to traditional methods. The technique shows promise for personalized prevention and treatment strategies by detecting and quantifying an individual's accumulated cardiovascular damage.
A new CNIC study warns that mitochondrial therapeutic interventions can cause damage due to the mixing of mitochondrial DNAs from two distinct origins. This can lead to medium- and long-term health issues, including heart failure, pulmonary hypertension, and muscle loss.
Researchers have identified a crucial nuclear transport mechanism essential for organ growth and development, involving the protein YAP. The study shows that YAP interacts with importin-7 to control its nuclear entry, regulating cell and tissue growth, and potentially targeting diseases such as atherosclerosis and cancer.
Researchers at the CNIC have identified a specific type of neutrophil behavior that predicts cardiovascular disease. The study provides crucial information for developing targeted therapies to minimize the consequences of myocardial infarction.
Researchers at CNIC have identified the essential role of GPR126 in placental development, revealing its critical function in fetal growth and viability. The study also highlights a possible link between GPR126 dysfunction and pregnancy complications such as preeclampsia.
Researchers from the CNIC and CIBERCV have created an animal model of HGPS, allowing them to study its effects and test treatments. They found that suppressing progerin expression and restoring lamin A can increase life expectancy by up to 84.5% in mice with mild symptoms, even if treatment is started late.