We are a multidisciplinary team of scientists who use biochemistry, biophysics and single-molecule techniques to understand the mechanics of the heart tissue and its regulation in health and disease.
The World Health Organization has estimated that cardiovascular disease (CVD) will by 2020 be the main health and socio-economic problem worldwide, in part due to the progressive aging that the world population is experiencing. Atherosclerosis and heart failure contribute significantly to CVD-related morbimortality in the elderly.
Blood vessels are not simply conduits for the body’s fluids; they also control essential biological responses and are an important therapeutic target in cancer and cardiovascular diseases.
Heart attack and many cases of ischemic stroke is the result of atherosclerosis; an extremely widespread disease that attacks arteries of humans all over the world. Our research group is devoted to finding new ways of preventing the development of dangerous atherosclerosis, and we focus on two key challenges that currently limit our ability to combat the disease.
Our research into cardiovascular disease is based on a simple principle: create to understand, create to treat.
The group has a strong connection with clinical research in different fields including atherosclerosis, acute coronary syndromes, acute and chronic heart failure, pulmonary hypertension, cardiovascular ageing and frailty, valve heart disease, advanced cardiovascular imaging, genetic and familial CV diseases.
We are interested in the molecular mechanisms that regulate cardiovascular development, homeostasis and disease. Most of our effort centers on the study of the Notch pathway.
Signals are the language of life, mediating the communication essential for cells proper behavior.
Our laboratory researches the mammalian mitochondrial electron transport chain (MtETC) and H+-ATP synthase, which together constitute the oxidative phosphorylation (OXPHOS) system.
The laboratory focuses on investigating from a multidisciplinary approach, the mechanisms underlying cardiac arrhythmias that occur in highly prevalent cardiovascular diseases in the general population, as well as in specific subsets at particular risk of sudden cardiac death.
Investigators Valentín Fuster, Javier Sanz (CNIC, Icahn School of Medicine at Mount Sinai), José María Castellano (CNIC, Hospital Universitario HM Monte Príncipe), Antonio Fernández-Ortíz (CNIC, Hospital Clínico San Carlos), Leticia Fernández Friera (CNIC, Hospital Universitario HM Monte Príncipe), Beatriz López-Melgar (CNIC, Hospital Universitario HM Puerta del Sur), Inés Garc
Grupo de reciente creación. En breve, publicaremos toda la información al respecto.
Angiogenesis, the formation of new capillaries, is closely linked to inflammation.
Our laboratory is interested in the biology of inflammation and immune cells.
Our laboratory focuses on the study of myocardial diseases, ranging from ischemia/reperfusion to heart failure. Our studies span the molecular origins of disease and their manifestations at the macro-anatomical and physiological levels, and our group includes experts in molecular biology, clinical cardiology and cardiovascular imaging.
The cardiac arrhythmia laboratory, led by José Jalife, has joined the CNIC in September 2014.
Our lab studies the molecular mechanisms that regulate the development of heart failure. Heart failure is the ultimate consequence of heart disease and it basically represents the inability of the heart to pump blood in an efficient manner due to the lack of proper heart contraction or relaxation.
The central research aim of the CNIC Functional Genomics Research Group is to understand how genome activity is regulated during development and how it contributes to human disease. For this, our projects are aimed to search for and identify distal acting cis-regulatory sequences, and elucidate how they act on their target genes.
Understanding peripheral mechanisms operating in autoinmmune and chronic inflammatory diseases is critical for the design and development of novel therapies against these immunological disorders.
The epicardium is a unicellular epithelial layer of that envelops the myocardium. It derives from the proepicardium (PE), a group of cells that arises at the inflow tract of the forming heart. PE cells attach to the myocardium and form an epithelial covering, called the epicardium.
Our group aims to understand the cellular and molecular mechanisms regulating striated muscle regeneration and growth in physiology and pathology, as well as in aging.
Sudden cardiac death (SCD) is a leading cause of death in western countries: coronary artery disease is the major cause of SCD in older subjects while inherited arrhythmogenic diseases are the leading cause of SCD in younger individuals.
B lymphocytes are key players of the immune response, mostly through the generation of a hugely diverse repertoire of protective antibodies.
Many important biological processes, including the regulation and development of the immune and cardiovascular systems, are regulated by the calcineurin (CN)/NFAT pathway. Much of our previous work relates to molecular interactions of CN with substrates. We are now studying the regulation and function of this pathway in inflammation, cardiovascular and inflammatory diseases.
Nuclear hormone receptors constitute a superfamily of ligandactivated transcription factors with diverse roles in development and homeostasis..
Metabolic syndrome is a medical disorder defined by the co-occurrence of obesity, impaired glucose tolerance, dyslipidemia and hypertension.
Intercellular communication is fundamental to the innate and adaptive immune responses.
Dendritic cells (DCs) are key immune sentinels that initiate and modulate immunity and tolerance. Manipulation of DCs holds promise as a potent immunotherapy tool for many diseases with an immune component, including infectious diseases, cardiovascular diseases, autoimmune diseases, and cancer.
We are interested in understanding the cellular basis of developmental processes and how this is controlled by transcription factor networks (TFN). We have developed genetic methods in the mouse that allow us to trace cell lineages using clonal analysis or functional mosaics.
Our group works on the development of high-throughput quantitative approaches for the dynamic analysis of the deep proteome, which are being applied to basic and translational projects in the cardiovascular field.
