Earlier detection of cardiovascular disease is a step closer thanks to the findings of team of CNIC scientists led by Francisco Sánchez-Madrid and Pilar Martín. The researchers found that the expression level of the molecule CD69 in blood cells inversely predicts the appearance of subclinical atherosclerosis (developing before symptoms appear) independently of classical cardiovascular risk factors. The results, published in Circulation, show that the expression of CD69 in circulating lymphocytes correlates inversely with the presence and extent of subclinical atherosclerosis.

The origin of atherosclerosis and its progression to acute myocardial infarction and stroke involve an essential contribution from the inflammatory immune response. However, according to Francisco Sánchez-Madrid, “The relationship between lipid metabolism and the immune response is not well understood. The established hypothesis is that oxidized low-density lipoproteins (LDLox) induce the recruitment of inflammatory immune cells and their accumulation in the plaque; however, there is also evidence that cells and tissues can respond to LDLox by inhibiting proinflammatory signals.”

People who sleep fewer than 6 hours a night may be at increased risk of cardiovascular disease compared with those who sleep between 7 and 8 hours, suggest the results of the PESA CNIC-Santander Study published in the Journal of the American College of Cardiology (JACC). The study indicates that poor-quality sleep increases the risk of atherosclerosis—the build-up of plaque in the arteries throughout the body.

The researchers explained that “this new study emphasizes that we need to include sleep as one of our weapons in the fight against heart disease—a factor that is neglected in our society every day. This is the first study to show that objectively measured sleep is independently associated with atherosclerosis throughout the body, not just in the heart.”

The immune response to our intestinal microbiota ensures that these microorganisms remain in their proper place. When the intestinal immune barrier is damaged, the gut bacteria can spread and cause inflammation throughout the body. Now, a study by scientists from the CNIC and the Universidad Complutense in Madrid reveals a new mechanism in the regulation of this immune barrier.

The study, published in Immunity, identifies a mechanism through which intestinal bacteria such as Lactobacillus strengthen the intestinal barrier to support a mutually beneficial relationship and prevent inflammation. The results have potential implications for the treatment of diseases featuring the spread of commensal bacteria outside the gut, as occurs in some metabolic disorders.

The research team propose that a new treatment strategy for these conditions could be the use of probiotics (‘beneficial’ intestinal microorganisms) or prebiotics (nutrients that promote the growth of beneficial microorganisms); however, the mechanisms underlying this strategy are so far unknown.

CNIC scientists have demonstrated the existence of an immune “clock” that coordinates the day/night cycles through the activity of a class of leucocytes called neutrophils. Neutrophils constitute the body’s main line of defense, but their action can also damage healthy cells of the cardiovascular system. This newly discovered clock determines when neutrophils are activated and when it is time to eliminate them from the circulation. First author José María Adrover explained that the researchers have identified “a series of molecules in the neutrophil nucleus and cell membrane that respond to diurnal (circadian) patterns in lightness and darkness and regulate the migration and localization of neutrophils in the body.” The study was carried out by the CNIC research group led by Andrés Hidalgo and is published in Immunity.

Due to the worldwide high prevalence of infectious and cardiovascular diseases, the study could have wide-ranging clinical implications. The team is currently working on ways to manipulate this immune clock with drugs to induce diurnal or nocturnal immunity, depending on the needs of each patient. This therapeutic approach could be valuable for people at risk of cardiovascular events and for immune-compromised patients susceptible to infection.

Researchers at the CNIC identified a very early marker of cardiac damage in patients undergoing therapy with anthracyclines, a family of drugs commonly used to treat cancer. This finding will enable the early diagnosis of the cardiotoxicity associated with this group of widely used chemotherapy drugs.

Dr Borja Ibáñez coordinated the study, published in the Journal of the American College of Cardiology (JACC). As Dr Ibáñez explained, the results have important implications for therapy because the detection this drug-induced damage at very early stages will permit “the implementation of treatments to prevent further deterioration in heart function and a clinical management more closely adapted to the needs of each patient.” The identified marker is affected much earlier than any of the markers used in current clinical practice.

Researchers at the CNIC and the Universidad de Oviedo have discovered a new molecular mechanism involved in the premature development of atherosclerosis in mice with Hutchinson-Gilford progeria syndrome (HGPS). The results, published in EMBO Molecular Medicine, identify a potential therapeutic target for this severe genetic disease.

The study, co-directed by Vicente Andrés of the CNIC and the CIBERCV and Carlos López Otín of the Universidad de Oviedo, identifies a molecular mechanism involved in the accelerated development of atherosclerosis in progeria. In addition, the results identify a pharmacological treatment that slows the progression of atherosclerosis and extends the lifespan of progeroid mice.

The study, featured in an editorial in the journal, shows for the first time that “stress in the endoplasmic reticulum (ER stress) and the associated unfolded protein response (UPR) are involved in the death of vascular smooth muscle cells in progeroid mice,” explained first author Magda Hamczyk.

Using advanced PET/MRI technology, researchers at the CNIC have detected arterial inflammation in regions that have yet to develop atherosclerotic plaques. These results from the PESA-CNIC-Santander study were published in JACC. The research team used this innovative technology to analyze the inflammatory process in the arteries of a group of people who had already developed atherosclerotic plaques.

The results show that inflammation is present at early stages of atherosclerosis, above all in regions that have not developed plaques. The study also shows that this arterial atherosclerosis can be an early indication of the later appearance of plaques that underlie cardiovascular disease and events such as heart attack and stroke. The researchers are currently analyzing the role of arterial inflammation in this process; this information will help to establish early diagnosis and develop new anti-inflammatory therapies for this disease.

A team at the CNIC has found an explanation for the lower rate of liver cancer in women. The answer lies in the hormone adiponectin, which is produced in higher amounts in women than in men and protects the liver against the development of the main form of liver cancer, hepatocellular carcinoma. In their quest to understand why people with obesity have a higher risk of developing liver cancer, the CNIC research group led by Guadalupe Sabio found that adiponectin is more abundant in women and slim people. The study, published in the Journal of Experimental Medicine, shows that adiponectin protects the liver against the development of hepatocellular carcinoma.

The research team showed that adiponectin, a hormone produced by adipose tissue, has an anticancer effect in the liver. In a group of healthy individuals, the team found that women produce more adiponectin than men. Describing the study, Dr. Sabio commented, “the circulating levels of adiponectin decline with the development of obesity and after puberty in men, and these are precisely the populations with higher rates of liver cancer. This observation prompted us to study the phenomenon in depth.”

A research team at the CNIC led by Guadalupe Sabio has discovered that the protein p38g, one of the four types of p38 kinase, is essential for the initiation of cell division in liver cells. This indicates that “p38g could be a useful therapeutic target for liver cancer,” said Sabio, adding, “we are now developing inhibitors of this protein to test in this cancer.” The study was published in Nature. The four members of the p38 kinase family are so similar that at first they appear to have overlapping or redundant functions. Detailed analysis of their three-dimensional structures revealed that one of the four, p38g, also shares close similarities with another family of proteins called CDKs. These proteins are well-known regulators of cell division and the cell cycle and play a well-established role in the development of cancer.

Children may have a better chance of avoiding unhealthy habits linked to obesity and cardiovascular disease later in life if they are taught properly about healthy behaviors in preschool, CNIC researchers have shown in a first-of-its-kind study.

The researchers focused on children living in a socioeconomically disadvantaged community, a situation frequenly linked to higher rates of obesity, heart disease, and other health issues. Valentin Fuster created and led the trial, called the FAMILIA Project at Mount Sinai Heart. The results were published in the Journal of the American College of Cardiology.

“Results from this new study prove that early intervention is effective in preschool-age children, but we believe this can also promote healthy behaviors among their caregivers and teachers and have a far-reaching impact”, explained Dr Fuster.

Scientists of the CNIC led by Rui Benedito discovered a cellular and molecular mechanism that can be exploited to induce productive and sustained angiogenesis in tissues that have become ischemic due to reduced blood supply.

Until now, tissue regeneration treatments based on vascular growth factors have not succeeded in inducing effective angiogenesis—the process through which the body generates new blood vessels. The new results, published in Nature Communications, suggest that it might be possible to manipulate the newly discovered mechanism to achieve optimal therapeutic angiogenesis.

Scientists of the CNIC led by Rui Benedito have developed a new genetic tool (iSuRe-Cre) that provides certainty in Cre-inducible genetic modifications, a key technique for understanding gene function.

Most analysis of gene function in biomedical research relies on the use of Cre-lox technology. Cre-Lox technology allows the regulation of gene expression at any time or in any cell type thanks to the ability of the Cre recombinase protein to recognize and recombine lox sites introduced at specific locations in the mouse genome, leading to the deletion of the genes being studied. Despite the major impact of Cre-loxP technology on biomedical research, numerous studies have demonstrated the need for caution in its use. The main problem is that the Cre activity level is often insufficient to fully recombine and eliminate expression of the target gene, generating uncertainty about whether the desired genetic modification has been achieved. To overcome this technical hurdle, the CNIC team developed an innovative method based on a new allele called iSuRe-Cre. iSuRe-Cre is compatible with all existing Cre/CreERT2/lox alleles and guarantees high Cre activity in the cells that express the fluorescent reporter. This ultimately increases the efficiency and reliability of the analysis of Cre-dependent gene function. Moreover, the use of the new iSuRe-Cre mice permits the induction of multiple genetic deletions in the same cell. This important property allows the study of functional genetic interactions or epistasis—how the function of one or more genes depends on the function of another.

A team of scientists led by Dr Enrique Lara Pezzi at the CNIC identified the RNA-binding protein SRSF3 as an essential factor for proper heart contraction and survival. In a study published in Circulation Research, the researchers found that loss of cardiac expression of SRSF3 leads to a critical reduction in the expression of genes involved in contraction. Knowledge of the mechanism of action of SRSF3 in the heart could open the way to the design of new therapeutic approaches for the treatment of heart disease. The identification of mRNA capping as a mechanism that protects against the development of systolic heart failure could open the way to the development of urgently needed therapeutic tools to combat this disease.

Ortiz-Sanchez, P., Villalba-Orero, M., Lopez-Olaneta, M. M., Larrasa-Alonso, J., Sanchez-Cabo, F., Marti-Gomez, C., Camafeita, E., Gomez-Salinero, J. M., Ramos-Hernandez, L., Nielsen, P. J., Vazquez, J., Muller-McNicoll, M., Garcia-Pavia, P., & Lara-Pezzi, E. (2019). Loss of SRSF3 in Cardiomyocytes Leads to Decapping of Contraction Related mRNAs and Severe Systolic Dysfunction. Circulation Research, 125(2), 170-183. doi:10.1161/CIRCRESAHA.118.314515

The CNIC coordinated the first international consensus document providing guidelines on the conduct of magnetic resonance imaging studies after a myocardial infarction in clinical trials or experimental models. The document concludes that the main outcome parameter in studies assessing new treatments should be absolute infarct size—the percentage of the left ventricle that is irreversibly damaged. The recommended timing for magnetic resonance imaging is between 3 and 7 days after the infarction.

The document, coordinated by Dr Borja Ibáñez, addresses the need within the cardiovascular community for guidance on the best protocols, the best techniques, and the most appropriate situations for conducting a magnetic resonance imaging study after a heart attack. The document was published in the Journal of the American College of Cardiology (JACC).

Scientists at the CNIC and Puerta de Hierro Majadahonda Hospital have discovered a possible treatment for arrhythmogenic right ventricular cardiomyopathy type 5 (ARVC5), a fatal genetic disease for which there is unfortunately no cure. The research team, whose findings were published in Circulation, showed that strategies to inhibit the protein kinase GSK3 in transgenic mice with ARVC5 reduce fibrosis and improve heart function.

The research team tested several candidate therapeutic approaches in the mouse ARVC5 model. While treatments directly targeting fibrosis were ineffective, positive results were obtained with two strategies for inhibiting GSK3, one based on pharmacological inhibition and the other on overexpression of the calcineurin subunit CnAβ1.

Researchers at the CNIC, the Hospital Clínico San Carlos in Madrid, and the Spanish cardiovascular research network (CiberCV) discovered a new method to optimize ablation of atrial fibrillation (AFib), one of the most common forms of irregular heartbeat (arrhythmia). The study was featured on the cover of the journal Circulation Research.

The new method allows ablation procedures to be tailored to the specific needs of individual patients with persistent AFib, identifying the key regions to treat with high precision. Moreover, the method costs no more than the conventional procedure and there is thus no obstacle to its use by most centers experienced in AFib ablation.

The investigators propose that the new algorithms could be easily incorporated into conventional electroanatomical navigation systems, increasing the precision and reducing the cost of patient-specific procedures for the ablation of persistent AFib.

Quintanilla, J. G., Alfonso-Almazan, J. M., Perez-Castellano, N., Pandit, S. V., Jalife, J., Perez-Villacastin, J., & Filgueiras-Rama, D. (2019). Instantaneous Amplitude and Frequency Modulations Detect The Footprint of Rotational Activity and Reveal Stable Driver Regions as Targets for Persistent Atrial Fibrillation Ablation. Circulation Research, 125(6), 609-627. doi:10.1161/CIRCRESAHA.119.314930

CNIC scientists have found that that a higher rate of coronary revascularization during hospitalization for non-ST segment elevation acute coronary syndrome (NSTEACS) is associated with better patient survival 2 years after hospital discharge, whether analyzed at the hospital, national, or supranational level.

The article was published in the Journal of the American College of Cardiology, and CNIC researchers Héctor Bueno, Xavier Rosselló, and Stuart Pocock believe that the findings will help to define and update quality-care guidelines for acute myocardial infarction, such as those recommended by the Acute Cardiovascular Care Association of the European Society of Cardiology. The revascularization rate in patients admitted for NSTEACS can serve as an index of health-care quality at the hospital, national, or supranational level. The CNIC researchers also affirmed that these results highlight “the importance of addressing the mismatch between clinical practice guideline recommendations and common medical practice.”

CNIC researchers have defined the dynamics of the transfer of mitochondrial DNA, a type of genetic material, from mothers to their offspring. The study was published in Cell Metabolism. Using experimental mouse models, the research team led by Dr José Antonio Enríquez found that when the mother’s cells contain more than one mitochondrial DNA variant, this genetic transfer from mother to pup is controlled by two mechanisms: first during the development of the egg (oocyte), and later during the early stages of embryonic development. The scientists explained that “this control is aimed at preventing the co-occurrence of various types of mitochondrial DNA in the new individual,” which can lead to the development of mitochondrial diseases.

The information provided in the new study is important for two reasons. Understanding the mechanisms that regulate the segregation of the mitochondrial genome is necessary for the development of strategies to prevent mother-to-child transfer of mutated mitochondrial DNA that cause mitochondrial diseases. The new findings will also help scientists to devise ways to prevent different types of mitochondrial DNA co-occurring in the same cell as an unwanted result of medical interventions; this phenomenon, known as heteroplasmy, is a potential risk of mitochondrial replacement therapy.

Scientists at the CNIC have identified a possible treatment for Alzheimer disease. Working together with a scientific team at The Rockefeller University in New York, the investigators have shown that treatment with the oral anticoagulant dabigatran delays the appearance of Alzheimer disease in mice.

The results, published in the Journal of the American College of Cardiology, show that after a year of treatment with dabigatran, mice had no memory loss and no reduction in cerebral circulation. This treatment also reduced typical Alzheimer symptoms, including cerebral inflammation, blood vessel injury, and amyloid protein plaques.

Scientists at the CNIC have identified the molecular mechanisms that allow our cells to adapt to, protect themselves against, and survive mechanical stress. The results, published in Nature Communications, show that our cells produce molecules that act as a type of ‘airbag’ in response to mechanical stress. Without this protective and adaptive system, the heart, an organ subject to continuous mechanical forces, “would be unable to correctly perform its blood-pumping role,” explained lead author Miguel Ángel del Pozo. First author Asier Echarri added that the findings “show the importance of identifying the molecular mechanisms that protect cells against mechanical stress.”

The findings are important because knowledge about how cells are protected against mechanical stress “will give us a better understanding of the molecular basis of diseases such as some forms of muscular dystrophy, cardiomyopathies, and lung or vascular diseases characterized by sensitivity to physical activity. The findings will also shed light on the mechanisms of injury to organs with a high level of mechanical activity, such as the heart, lungs, muscles, and blood vessels.”

Research into new endogenous mechanisms of tissue regeneration is an innovative research avenue in cardiac regeneration. This is the central goal of the REANIMA project (New‐generation cardiac therapeutic strategies directed to the activation of endogenous regenerative mechanisms), a research program coordinated by Dr Miguel Torres at the CNIC and supported by €8 million funding over 5 years, of which €1,380,000 is directly managed at the CNIC. The project started in January 2020.

The project brings together knowledge obtained from species that can regenerate their hearts (fish and amphibians), animals that cannot (adult mammals), and human heart tissues generated by tissue engineering.

REANIMA is the first Europe-wide project to integrate basic research findings in an effort to transform them into medical applications in the field of cardiac regeneration. REANIMA is funded by the European Union’s Horizon 2020 research and innovation programme under grant agreement nº 874764. Project activities range from identifying new targets in animal models to the design of clinical trials. The project is linked to the similarly named ‘REANIMA-CM’ project funded by the Comunidad de Madrid, which is also coordinated by Dr Torres.

Curing disease with neutrophils; this is the goal of the NeutroCure project. How will that work? “Neutrophils have a yin yang character,” explains Andrés Hidalgo, whose team at CNIC is one of six member groups participating in this project coordinated by Andriy Mokhir Friedrich at Alexander University, Germany.

NeutroCure focuses on reactive oxygen species (ROS) produced by neutrophils. In healthy organisms, ROS play crucial roles, such as signaling to regulate cell growth, providing the trigger for the formation of neutrophil extracellular traps, and modulating inflammation. However, high ROS concentrations damage tissues, and nature has therefore evolved precise mechanisms to control ROS duration and concentration and to ensure that these molecules remain confined to locations close to their targets.

Professor Jacob Fog Bentzon of Aarhus University and the CNIC has received €2 million from the European Research Council for a ground-breaking research project on atherosclerosis, one of the most frequent causes of death in the world.

Although atherosclerosis is a very common disease, much work remains to be done to define exactly what happens when fat and cholesterol are deposited in the walls of arteries, which leads to arteriosclerosis and the risk of blood clots in the heart and the brain.

Scientists only recently discovered that many of the cells found in atherosclerotic plaques are in fact vascular smooth muscle cells that have altered their appearance and function. The research group led by Professor Fog Bentzon will use the new funding to uncover the significance of these mysterious cells.

Two CNIC projects were selected by the Fundación Bancaria La Caixa for its Proyectos de Investigación en Salud program for 2018.

The projects are ‘Dysfunction of Ion Channel Complexes in Inheritable Cardiac Diseases’, led by Dr José Jalife, and ‘Nitric Oxide signaling and proteoglycans in Marfan syndrome aortopathy: mechanisms and new therapeutic targets’, led by Dr Juan Miguel Redondo.

Dr Jalife’s project adopts pioneering approaches to define the causes of sudden cardiac death in inherited cardiac diseases and identify new and more effective prevention strategies. The new techniques employed in the study include the injection of adeno-associated virus to target mutated genes to the heart cells of mice, the derivation of cardiomyocytes from human induced pluripotent stem cells, and advanced proteomics and bioinformatics approaches. The project was awarded €499,895.

CNIC postdoctoral researcher Ivana Nikolić has been awarded funding for 2 projects by the European Foundation for the Study of Diabetes (EFSD) to study the role of T cells in the development of diseases associated with obesity. The 2 awards are the EFSD–Lilly Young Investigator Award, providing €50,000 and the EFSD Rising Star Fellowship, bringing another €30,000. Dr Niković previously obtained the 2017 EFSD–Lilly Research Fellowship Award, receiving a grant of €50,000.

Dr Nikolić obtained her PhD in Immunology at the University of Belgrade in 2014. In 2015 she joined Dr Guadalupe Sabio’s lab at the CNIC with an FP7-People Marie Sklodowka - Curie Actions, MSCA - COFUND talent recruitment fellowship. These fellowships were intended to attract outstanding foreign scientists to the CNIC at an intermediate stage in their career so that they could develop their research in Spain.

The Minstry of Science, Innovation and Universities awarded the 2019 Gregorio Marañon National Research Prize to Valentín Fuster. The jury panel awarded the prize to Dr Fuster in recognition of his unparalleled research record and his enormous contributions to the prevention, diagnosis, and treatment of cardiovascular disease. The National Research Prize, first awarded in 1982, is the highest Spanish accolade for scientific research. The aim of the award is to reward the achievements of Spanish scientists who are international leaders in their research fields and who make exceptional contributions to the advance of scientific knowledge, technology transfer, and human progress.

CNIC group leader Dr Pura Muñoz-Cánoves was awarded the XXXI Rei Jaime I prize in the Medical Research category. The Rei Jaume I are awarded to people who have made outstanding contributions in their fields through work carried out mostly in Spain. The prizes are awarded annually, and each prize winner receives a gold medal, a diploma, and €100,000, on the condition that part of this money be used to fund research and enterprise in Spain.

The prize was awarded to Dr Muñoz for her work on the molecular mechanisms of aging, especially the progressive changes that take place in the stem cells of animals as they age and the possibility of manipulating these changes for regenerative medicine. Dr Muñoz was also awarded the Lilly Foundation Preclinical Biomedical Research Prize for 2019 in recognition of her pioneering work on tissue regeneration.

CNIC researcher Dr Rodrigo Fernández Jiménez received the 2019 Marie Skłodowska-Curie Actions Award in the ‘Scientific Careers for Policymaking’ category for his Comprehensive Lifestyle Intervention Project (CLIP).

CLIP investigates new approaches to health promotion and disease prevention. The goal is to help policy makers devise effective strategies to promote a healthy life style among children.

The aim of the project is to convince governments that low-cost and side-effect–free health-promotion programs aimed at young people provide a potentially effective way to reduce the cardiovascular disease epidemic if integrated into national school curriculums.

CNIC researcher Dr Sara Cogliati was awarded one of 5 prizes in the XIV edition of L’Oréal-Unesco For Women in Science Program for her project investigating sex-specific characteristics in cardiovascular disease. This research is crucial to finding effective treatments for heart failure in women because historically most treatments have been based on research in men, despite important differences between the sexes in the way the disease manifests. Dr Cogliati’s research signals an important advance toward gender equality in the treatment of disease.

CNIC group leader Dr Miguel Torres has been elected a member of the European Molecular Biology Organization (EMBO). In the words of EMBO Director Maria Leptin, “EMBO members are expert scientists who carry out pioneering research across all disciplines in the life sciences, from computer models or analysis of individual molecules and cell mechanisms to the study of higher-level systems in development, cognitive neuroscience, and evolution.”

Dr Miguel Torres’s research focuses on the regulation of embryonic development and the formation and regeneration of organs. He has made major contributions to the understanding of how gene activities regulate regionalization processes in the developing embryo and the discovery of mechanisms involved in quality control and organ regeneration.

Professor Francisco Sánchez Madrid was awarded an honorary doctoral degree by the University of Córdoba. Dr Sánchez Madrid heads the Intercellular Communication in the Inflammatory Response laboratory at the CNIC and is full professor in Immunology at Madrid Autonomous University and Scientific Director of the Research Institute and Hospital de La Princesa, Madrid.

For Semana de la Ciencia 2019, the CNIC introduced 2 new activities. The ‘Family Day at the CNIC’ event was designed especially for younger children and their families, while the #ConCienciaCNIC one-day events consisted of scientific workshops for children with special needs.

These activities catered for children between the ages of 4 and 14, accompanied by adults, and aimed to introduce tomorrow’s scientists to the world of research. Through theater, play activities, and scientific workshops, the children had fun, but also learned from the experiments carried out by CNIC volunteers.

The CNIC and the Spanish Society of Cardiology (SEC) joined forces to launch a pioneering clinical trial in Spain: TREatment with Beta-blockers after myOcardial infarction withOut reduced ejection fracTion (REBOOT). In the words of prinicipal investigator Dr Borja Ibáñez, “the ambitious aim of this trial is to change clinical practice guidelines for the treatment of acute myocardial infarction.” The trial will test the effect of maintaining beta-blocker therapy after hospital discharge in a cohort of 8500 patients.

Beta-blockers are drugs that reduce heart rate, blood pressure, and cardiac contractility (strength of contraction). This promotes cardiac diastole (filling), which improves heart function and blood flow in the coronary arteries. Most of the evidence supporting the use of beta-blockers in heart attack patients comes from before the current era of widespread use of reperfusion therapy. Despite this, the recommendations in European and American guidelines for beta-blocker therapy in these patients have remained unchanged for decades.

REBOOT will be the first trial in the reperfusion era to study if the administration of beta-blockers after an acute myocardial infarction influences the incidence of death, reinfarction, and hospital readmission for heart failure. The trial will randomize 8500 patients to receive beta-blocker therapy or no beta-blocker therapy. Participants will be followed up for a minimum of 2 years and a maximum of 3 years. Outcome measures will include the incidence of clinical events and adherence to the randomized therapy, recorded at 13, 15, and 36 months. A subsample of 1000 patients will be assessed for quality of life during follow-up.

This research topic is of such high relevance that another 3 European trials similar to REBOOT are planned, in Sweden, Norway, and Denmark. In total, more than 20,000 patients with similar characteristics will be randomized to beta-blocker therapy or no beta-blocker therapy after a myocardial infarction with ventricular dysfunction.

Pro-CNIC Foundation President Luis de Carlos and General Secretary of Scientific Coordination Rafael Rodrigo formalized an agreement to renew the commitment of this body of 12 private companies to support the CNIC until 2028. The Pro-CNIC Foundation is an innovative example of public-private collaboration that has allowed the CNIC to establish itself as a world leader in biomedical research, contributing to the CNIC gaining Severo Ochoa accreditation in recognition of its international research excellence. Through the Pro-CNIC Foundation, 12 leading Spanish companies channel their business knowhow and financial support to the CNIC, representing a benchmark in successful scientific patronage. The companies participating in the Pro-CNIC Foundation are Acciona, Santander Bank, BBVA Bank, Endesa, the Mapfre Foundation, the Mutua Madrileña Foundation, the Ramón Areces Foundation, the Repsol Foundation, Inditex, “la Caixa”, Prisa, and Telefonica.

The Pro-CNIC Foundation enables the CNIC’s research to have a direct impact on patient care and health improvements in the general population. The Pro-CNIC Foundation also helps in the conversion of innovations into patents that generate an economic return and support research and development in Spain.

A heart attack survivor is donating the proceeds from her book to the CNIC after ‘coming back to life’. On July 14, 2014, Paula Elena Ramos came back from the doors of death. Without warning, and with no family history or prior symptoms, Paula Elena had a third-degree atrioventricular block. She tells her story in her book a“Historia del corazón que sembró una galaxia en un cuerpo eléctrico,” and all income from the sale of the book are being donated to arrhythmia research at the CNIC, specifically in the Advanced Development in Arrhythmia Mechanisms and Therapy laboratory led by Dr. David Filgueiras.

AAs part of the activities program linked to the V Congress of Scientist-Entrepreneurs in May, a group of participants spent a day at the CNIC learning about the center’s activities and installations.

The visited facilities included the Advanced Infrastructure for Translational Imaging (TRIMA), part of the ICTS Distributed Biomedical Imaging Network (ReDIB).

Training is one of the CNIC’s core activities, and the Center has devised a comprehensive training plan, the CNIC-Joven Training Plan. This global plan includes programs for participants at all levels, from high-school students to postdoctoral researchers and MDs. The CNIC-Joven Training Plan aims to fulfill the personal goal of Valentín Fuster “to attract and train the brightest young people from the earliest ages to create a pool of excellent researchers in the field of cardiovascular research.”

In 2019, 473 participants were enrolled on CNIC training programs.

The Acércate Program offers the highest-achieving senior high school students in the natural and health sciences the chance to experience life as a biomedical researcher, with the aim of awakening and strengthening interest in a biomedical research career.

Participants spend two weeks at the CNIC, learning modern techniques used in biomedical research, conducting supervised experiments, operating sophisticated scientific equipment and presenting the results of their work, all under the supervision of CNIC researchers.

Fellowships in 2019: 8

The CNIC collaborates with high schools of the Madrid Community in the following training programs:

4ºESO-CNIC: Sixteen life-science students from eight schools spent from 4 to 5 days at the CNIC laboratories exploring possible scientific careers.

The CNIC was also visited by 12 year-4 high-school students as part of the Programa 4ºESO+CNIC 2019. This program provides educational visits to businesses and observation sessions in a professional setting to students in their final year of compulsory secondary education. The aim is to promote a vocation for science among young students. The 12 students visiting the CNIC came from 7 high schools: IES Fortuny, IES Santa Teresa de Jesús, Colegio Raimundo Lulio, and Colegio Santa Francisca Javier Cabrini in Madrid and Colegio Humanitas de Torrejón de Ardoz, Colegio Gredos San Diego El Escorial, and Colegio Calasanz in Alcalá de Henares.

Practical experience for Technical School students: This program brought eighteen technical school students studying “Pathological and Cytodiagnostic Anatomy” and “Clinical and Biomedical Laboratory Science” to gain practical curricular experience in the CNIC’s laboratorios over a three-month period. Moreover, three students studying “Diagnostic Imaging and Nuclear Medicine” and “Clinical and Biomedical Laboratory Science” spent 10 months at the CNIC as part of the DUAL technical study program. The CNIC has signed collaborative agreements for this kind of interships with both DUAL Centers in Madrid offering courses in the Biomedicine field.

Cicerone Program

The Cicerone Program is open to advanced undergraduate students and Master’s students in biomedicine-related disciplines. Participants extend their scientific training through hands-on experience of laboratory-based biomedical research during the summer recess. In addition to carrying out a supervised research project, the students also attend CNIC seminars and workshops. The aim of the program is to give students first-hand knowledge of biomedical research so that they can make informed choices about the possibility of pursuing a scientific career.

Fellowships in 2019: 29

Curricular and Extracurricular University Practical Program

The CNIC offers practical training in cardiovascular research to visiting undergraduate students, including those on Erasmus internships.

Internships in 2019: 70 internships from 12 Universities, 4 of them outside Spain.

MASTERS AND GRADUATE STUDENTS

Master’s Fellowship Program (CNIC-ACCIONA) and Fundacion Carolina BBVA-CNIC Master’s Fellowship Program

These grants provide funding for students studying for a master’s degree at a Spanish university to conduct their experimental project (TFM) in a CNIC laboratory.

Fellowships in 2019: 15

Predoctoral (PhD) Program

The Predoctoral Program provides a unified framework for all CNIC researchers who are working toward a doctoral degree. All predoctoral researchers are signed up to this program, irrespective of their funding source. The aims of the program are to ensure uniform quality of predoctoral training at the CNIC and further to ensure fair and equal access of predoctoral researchers to training opportunities.

The Program schedules regular meetings between the predoctoral fellow and his or her thesis committee, composed of the thesis director, another CNIC group leader, and an external expert.

Graduate students at the CNIC awarded a PhD degree in 2019: 17

Graduate students studying for a PhD degree at the CNIC in 2019: 100

Insights into Research in Cardiovascular Disease Masters Module

This postgraduate course is run by the CNIC as part of the Universidad Autónoma de Madrid (UAM) Molecular Biosciences Master’s Program. This optional module provides a broad overview of cardiovascular biology, including perspectives from basic, clinical, and translational research.

Course participants are enrolled UAM Master’s students, CNIC predoctoral researchers, and participants on the Res@CNIC SEC Program (see below).