The REACT study reveals that 57.1% of participants aged 18 to 70 had atherosclerotic plaques, despite no symptoms or previous diagnosis. Most people with coronary atherosclerosis also had the disease in other arteries, making portable ultrasound devices a promising screening tool.
A study of 1,160 patients with dilated cardiomyopathy found that left ventricular hypertrabeculation is not associated with increased risk of heart failure, arrhythmias, or embolic events. The presence of hypertrabeculation does not modify clinical risk in any genetic subgroup.
A study led by CNIC suggests that intensive cardiac surveillance may have limited clinical value for lymphoma patients with low to moderate cardiovascular risk who are treated with anthracyclines. Nearly half of the patients met criteria for cancer therapy-related cardiac dysfunction, but most abnormalities were mild and transient.
A study by scientists at CNIC and UCLA reveals that mitochondrial calcium controls interaction between mitochondria and cellular fat stores. This regulation opens potential avenues for treating obesity and metabolic diseases.
A study led by the Centro Nacional de Investigaciones Cardiovasculares Carlos III has identified a new molecular mechanism involved in hypertrophic cardiomyopathy. Researchers confirm the effectiveness of mavacamten in treating the condition, regardless of genetic mutation type.
Researchers at CNIC developed a technique to analyze proteins in individual cardiomyocytes, uncovering new clues about cardiac regeneration. The study found that the transcription factor Myc alters protein expression differently in each cell, generating regenerative potential in a subpopulation of cardiomyocytes.
The European Research Council has awarded an Advanced Grant to CNIC researcher Florian Weinberger for the CARDIOSWITCH project, which aims to develop new regenerative strategies for congenital heart disease. The five-year project will investigate how mechanical workload influences cardiomyocyte proliferation and function.
Researchers found that mitochondria physically attach to nuclear pore complexes, delivering energy-rich molecules directly to the nucleus. This efficient system supports processes like gene regulation and cellular differentiation, and its disruption affects heart development and cellular function.
Researchers found that the right ventricle is better able to withstand loss of blood perfusion and oxygen supply during cardiac arrest, leading to longer preservation of its native electrical activity. The study's findings support the use of surface ECG signals to predict neurological recovery after hospital admission.
Researchers at CNIC identify mitochondrial complex I as a key checkpoint for dendritic cell activation. Restoring its function restores immune responses against viruses and tumors. The study paves the way for new strategies in vaccines and cancer immunotherapies.
Researchers discovered a biomarker that can predict disease progression and mortality in patients with severe heart failure. Mid-regional pro-adrenomedullin (MR-proADM) levels are associated with greater disease severity, mortality, and heart failure events.
Researchers found that active mitochondria keep dendritic cells ready to respond by maintaining key internal processes. Disrupting this balance alters DNA methylation patterns at regulatory regions, enabling rapid gene activation.
Researchers have found that remote ischemic conditioning can protect the heart without reducing antitumor efficacy in cancer patients undergoing anthracycline treatment. This non-pharmacological technique may reduce long-term cardiovascular complications and improve quality of life.
A yeast enzyme, Sc URA, has been found to sustain nucleotide synthesis independently of mitochondrial respiration in human cells. This discovery opens up new possibilities for treating mitochondrial diseases with no cure, and could provide a valuable experimental tool for understanding rare diseases and cancer.
Researchers identify non-contractile cell populations and their role in sustaining atrial fibrillation, a persistent and challenging-to-treat cardiac arrhythmia. The study provides insight into the cellular mechanisms involved and suggests new therapeutic strategies targeting these components.
A team developed a catheter-based approach to treat defective mechanical aortic valves, avoiding high-risk open-heart surgery. The procedure, known as mechanical valve-in-valve (ViMech), was successfully applied in three human patients with severely damaged mechanical valves and extremely high surgical risk.
A study published in Immunity reveals that type I interferons (IFN-I) help resolve inflammation by inducing changes in macrophage mitochondria, improving their ability to remove dead cells. The researchers found that treatment with IFN-I increases macrophage uptake of apoptotic cells and reduces the expression of inflammatory genes.
Researchers found that neutrophils, key immune cells, change their behavior in line with circadian rhythms, affecting cerebral perfusion and collateral circulation. This regulation influences stroke severity and patient recovery.
Research reveals that high blood pressure significantly increases risk of heart damage caused by anthracycline cancer treatments. The study identifies a 'perfect storm' effect when high blood pressure and anthracyclines coincide, leading to heart failure.
A new policy paper highlights five critical areas for advancing data-driven policymaking to curb the rising burden of non-communicable diseases in Europe. The paper emphasizes the need for inclusive data collection, solid governance, and real-time policymaking to address inequalities and ensure equitable healthcare.
A study by CNIC reveals that neutrophils, a type of immune cell, are less aggressive at night, resulting in less severe heart attacks. Researchers developed a pharmacological strategy to block the molecular clock in neutrophils, reducing their harmful potential during infarction.
Scientists created the first comprehensive map of neutrophils using next-generation sequencing technologies, revealing a stable architecture despite individual cells' short lifespan. This discovery opens new avenues for guiding immunity toward healing and facilitating translation to clinical studies.
A major analysis by CNIC and international institutions found beta-blockers offer no clinical benefit for patients with preserved cardiac function after myocardial infarction. The study analyzed data from five global clinical trials, confirming that beta-blocker therapy does not reduce the risk of death or cardiovascular events.
Researchers at CNIC developed a mouse model carrying a truncating FLNC mutation that reproduces the electrical abnormalities observed in patients. They then used CRISPRa-based gene-therapy to restore Filamin C protein production, reversing cardiac electrical abnormalities and arrhythmias.
Patients with genetic dilated cardiomyopathy who experience severe arrhythmias are at an elevated risk of developing advanced heart failure and requiring a heart transplant. Genetic mutations in genes associated with severe arrhythmias and sudden cardiac death increase the risk of serious heart failure complications.
A major new analysis from the REBOOT trial reveals that women treated with beta-blockers after a heart attack had a higher risk of death, reinfarction, or hospitalization for heart failure. The study also found that women presenting with infarction had a worse cardiovascular profile and a significantly worse prognosis than men.
A new clinical trial has found that beta-blockers, commonly prescribed for cardiac conditions, offer no clinical benefit for patients who have had an uncomplicated myocardial infarction. The REBOOT trial enrolled 8,505 patients and showed no significant differences between those receiving or not receiving beta-blockers in rates of deat...
A hospital imaging technique can monitor atherosclerosis by measuring cellular metabolism within arterial plaques. The study demonstrates that the FDG-PET signal reflects the metabolic activity of atherosclerotic plaques, enabling sensitive evaluation of treatment efficacy and disease progression risk.
A new study has identified a gut microbiota-derived metabolite, imidazole propionate (ImP), that appears in the blood during the early stages of active atherosclerosis. The presence of ImP is associated with the development of active atherosclerosis in people who otherwise appear healthy.
Researchers have uncovered the evolutionary logic of the OxPhos system and developed a tool to detect mutations causing mitochondrial disease. ConScore, a predictive index assesses clinical relevance of mutations in OxPhos proteins.
Researchers developed a new method to study mechanical proteins, revealing that disrupting protein titin causes muscle disease. The technique allows for targeted analysis of protein mechanics, paving the way for new therapeutic strategies.
Researchers at CNIC identify conventional type 1 dendritic cells as key players in driving atherosclerosis. They then develop an experimental therapy using immunosuppressive nanoparticles that successfully halt disease progression in animal models.
Researchers at CNIC uncover how the heart forms during earliest embryonic development, shedding light on congenital heart defects and regenerative medicine. The heart originates from two separate cell populations that coordinate their formation simultaneously.
Scientists have discovered a new immunotherapy strategy using type I dendritic cells to activate strong immune responses and generate immune memory against cancer. The treatment helps prevent tumor relapse in mouse models by triggering an immune memory response.
A team of researchers has developed a gene-therapy strategy to treat arrhythmogenic right ventricular cardiomyopathy type 5 (ARVC5), a rare and deadly hereditary disease. The treatment, using adeno-associated viruses, improved cardiac function and prolonged survival in mice with ARVC5-like disease.
Scientists have discovered that early-life cardiac injury in parents can alter heart development and function in offspring, leading to improved cardiac remodeling and increased blood ejection volume. This finding suggests a potential long-term impact on cardiovascular health.
Prof Silvia G. Priori recognized for groundbreaking research on cardiac arrhythmias, leading to novel treatments and therapies, including gene therapy approaches.
Researchers have identified a type of immune cell that produces extracellular matrix, strengthening the skin's defensive function and maintaining its integrity. This discovery may lead to new strategies for treating skin diseases, inflammation, diabetes, and age-related conditions.
Researchers at the CNIC have designed a treatment strategy to protect the heart against cardiotoxic effects of anthracyclines, a common class of anticancer drugs. Empagliflozin, an SGLT2 inhibitor, has been shown to preserve cardiac function and metabolism in experimental models.
Gut bacteria that cross a weakened intestinal barrier induce epigenetic changes in bone marrow, generating trained immune cells primed to respond more efficiently to infections. However, this amplified immune response also contributes to the development of inflammatory diseases such as cardiovascular and neurodegenerative conditions.
The CNIC has developed a comprehensive set of genetic tools and mouse lines called iFlpMosaics, enabling accurate investigation of somatic mutations on cellular biology and disease. This toolkit facilitates the study of complex interactions between cells within their microenvironment.
Researchers identify caveolae's role in protecting adipocytes from rupture and inflammation; this discovery opens new avenues for treating metabolic diseases like obesity. The study highlights the importance of the caveolin-1 protein in maintaining cellular integrity.
A new CNIC study identifies a surprising mechanism through which tissue viscoelasticity counteracts the sensing of rigidity. Cells respond to ECM viscoelasticity regulating response times and outweighing high-rigidity sensing.
A new image processing strategy for cardiac magnetic resonance imaging identifies areas responsible for complex ventricular tachycardias, enabling preoperative planning and reducing procedure times and complications. The systematic approach eliminates operator bias and increases sensitivity for detecting these regions.
A team of researchers has identified the activation of the YAP/TAZ pathway as a major contributor to atherosclerosis in patients with Hutchinson-Gilford progeria syndrome. This discovery sheds light on the vascular problems faced by HGPS patients and opens up potential new avenues for treatment.
A study published in JACC demonstrates that subclinical atherosclerosis burden and progression independently predict death from any cause. Asymptomatic individuals with high carotid plaque burden and coronary artery calcification are at increased risk of mortality.
Researchers at the CNIC found that respiratory complex I possesses sodium transport activity essential for efficient cellular energy production. This discovery provides a molecular explanation for Leber's hereditary optic neuropathy and may have implications for other neurodegenerative diseases.
A study finds that cardiometabolic indicators like metabolic syndrome and diabetes impair coronary microvascular function, increasing cardiovascular risk. The presence of subclinical atherosclerosis also contributes to altered microvessel function.
The RESILIENCE clinical trial explores the effectiveness of remote ischemic conditioning to prevent cardiotoxicity in lymphoma patients undergoing anthracycline-based chemotherapy. The trial aims to reduce heart failure prevalence and improve quality of life for cancer survivors.
Researchers at CNIC have identified endothelial-to-mesenchymal transition as a novel mechanism in premature atherosclerosis in progeria. The study proposes a new therapeutic target for this disease and highlights the importance of investigating rare diseases like progeria.