Proyectos - Internacionales - Programas de Investigación e Innovación de la UE
![]() | These projects have received funding from the European Union's Horizon 2020 research and innovation programme under grant agreement which is refrenced under each Project. |
Título:
Secondary prevention of Cardiovascular disease in the elderly trial
Acrónimo
SECURE
Convocatoria:
H2020-PHC-2014-two-stage
Referencia:
GA-633765
Investigador principal:
Valentín Fuster Carulla
Fecha inicio:
01/05/2015
Fecha fin:
31/12/2021
Presupuesto concedido:
1.465.972,00 €
Fuente de financiación:
EC-European Commission
Título:
Molecular strategies to treat inherited arrhythmias
Acrónimo
EU-rhythmy
Convocatoria:
H2020-ERC-2014-ADG
Referencia:
GA-669387
Investigador principal:
Silvia Priori
Fecha inicio:
01/11/2015
Fecha fin:
31/10/2021
Presupuesto concedido:
600.000,00 €
Fuente de financiación:
EC-European Research Council
Título:
Tissue regeneration and aging: the decisive quiescent stem-cell state
Acrónimo
STEM-AGING
Convocatoria:
H2020-ERC-2016-AdG
Referencia:
GA-741966
Investigador principal:
Pura Muñoz Cánoves
Fecha inicio:
01/11/2017
Fecha fin:
31/10/2022
Presupuesto concedido:
1.248.125,00 €
Fuente de financiación:
EC-European Research Council
Título:
Functional characterisation of mitochondrial metabolic adaptations to innate sensing in dendritic cell subsets
Acrónimo
MITOMAD
Convocatoria:
H2020-ERC-2016-CoG
Referencia:
GA-725091
Investigador principal:
David Sancho Madrid
Fecha inicio:
01/12/2017
Fecha fin:
30/11/2023
Presupuesto concedido:
1.995.000,00 €
Fuente de financiación:
EC-European Research Council
Resumen:
We are investigating how tissue damage and microbial signals lead to mitochondrial reprogramming in dendritic cells (DCs) and macrophages, and how manipulation of mitochondrial metabolism regulates myeloid cell function. This project aims to identify new targets to exploit DCs and macrophages for improved immunotherapy. So far we have: 1. Characterized the metabolic reprogramming after DC stimulation with different stimuli both in mouse and human DCs. 2. We are performing the analysis of how innate sensing connects with mitochondrial adaptations in DCs; 3. We have addressed the effect of drugs targeting mitochondrial biology and now we are analyzing the effect of genetic manipulation of mitochondrial biology on DC function in vitro. 4. We are assessing the functional in vivo effects of targeting mitochondrial biology in DCs in homeostasis and disease. The project aims 1. the analysis of how sensing of external stimuli by DCs leads to mitochondrial adaptations; 2. The investigation in how mitochondrial metabolism may impact in DC function. The main results obtained in these aims are: 1. In the current reporting period we have found how macrophage polarization is regulated by Fgr kinase-mediated phosphorylation of mitochondrial CII, which impacts on proinflammatory macrophages in the adipose tissue. Fgr deficiency leads to improved glucose metabolism and leaner mice with reduced liver steatosis (Acín-Pérez et al. Nat Metabolism 2020). In addition, we found that a polybacterial preparation induces metabolic reprogramming and trained immunity, protects against viral infection and enhances vaccine immunogenicity (Brandi et al. 2022. Cell Reports; del Fresno et al. Front. Immunol. 2021). 2. Our novel genetic approaches based on CD11c-selective deletion of key proteins affecting OXPHOS complexes have revealed diverse results depending on the targeted complex. We performed the analysis of CD11c-expressing macrophages. We found that distinct physiological functions direct the metabolic requirements of tissue-resident macrophages. Using the CD11c-Cre driver line, we observed a profound phenotype in some CD11c-expressing macrophage (MF) populations. Using our CD11c∆Tfam mice and Lysozyme M-Cre Tfamf/f (LysM∆Tfam) mice, we found that mitochondrial impairment differentially affects presence and identity of MFs correlating with their expression levels of OXPHOS-related genes. Alveolar macrophages are drastically affected and the oxphos is needed for macrophage lipid handling activity. Macrophages in tissues exposed to lipids in homeostasis are more dependent on oxphos for their metabolism. In addition, proinflammatory macrophages in the adipose tissue are also oxphos-dependent. Due to the lack of this proinflammatory macrophages, LysM∆Tfam mice are leaner and show better glucose metabolism and less liver steatosis than control mice (Wculek et al. submitted). In relation with the previous mentioned objectives, the progress and expected potential are: 1. We have characterized how innate stimuli lead to distinct metabolic signatures and have described modulatory mechanisms that affect metabolic reprogramming and trained immunity (Saz-Leal et al. Cell Reports. 2018). We found that a polybacterial preparation induces metabolic reprogramming and trained immunity, protects against viral infection and enhances vaccine immunogenicity (Brandi et al. 2022. Cell Reports; del Fresno et al. Front. Immunol. 2021).We are now working on new regulators of trained immunity with particular focus on the role of mitochondrial metabolism. 2. In our biased approach we have established the involvement of the HIF-1 pathway in alveolar macrophage function and the importance of sensing oxygen for terminal differentiation (Izquierdo et al. Cell Reports. 2018). We are also analyzing other sensing pathways that affect DC and macrophage mitochondrial metabolism. 3. We have found a new function in inflammation of DCs (Del Fresno et al. Science. 2018) and a new pathway of sensing microbiota that affects immunity in the gut (Martínez-López et al. Immunity. 2019). This has potential impact as new functional targets that can be affected by the manipulation of mitochondrial metabolism, and we are currently exploring this avenue. In fact, we have recently described that Fgr kinase can modulate mitochondrial complex II activity and macrophage polarization, which affects host metabolism. Fgr promotes proinflammatory macrophage polarization, obesity and metabolic syndrome (Acín-Pérez et al. Nat Metab. 2020). 4. Our work has established that cDC1s can be effectively used for cancer immunotherapy (Wculek et al. JITC. 2019). The potential is to manipulate metabolism in cDC1s to improve cancer immunotherapy.
Título:
Transgenerational epigenetic inheritance of cardiac regenerative capacity in the zebrafish
Acrónimo
TransReg
Convocatoria:
H2020-ERC-2018-CoG
Referencia:
GA-819717
Investigador principal:
Nadia Isabel Huber
Fecha inicio:
01/08/2019
Fecha fin:
31/07/2024
Presupuesto concedido:
326.250,00 €
Fuente de financiación:
EC-European Research Council
Título:
Novel mitochondria-targeting therapies for chemotherapy-induced cardiotoxicity
Acrónimo
Matrix
Convocatoria:
H2020-ERC-2018-CoG
Referencia:
GA-819775
Investigador principal:
Borja Ibáñez Cabeza
Fecha inicio:
01/09/2019
Fecha fin:
31/08/2024
Presupuesto concedido:
1.473.437,50 €
Fuente de financiación:
EC-European Research Council
Título:
New-generation cardiac therapeutic strategies directed to the activation of endogenous regenerative
Acrónimo
REANIMA
Convocatoria:
H2020-SC1-BHC-07-2019
Referencia:
GA-874764
Investigador principal:
Miguel Torres
Fecha inicio:
01/01/2020
Fecha fin:
30/06/2025
Presupuesto concedido:
1.380.000,00 €
Fuente de financiación:
EC-European Commission
Título:
Development of “smart” amplifiers of reactive oxygen species specific to aberrant polymorphonuclear neutrophils for treatment of inflammatory and autoimmune diseases, cancer and myeloablation.
Acrónimo
NeutroCure
Convocatoria:
H2020-FETOPEN-2018-2020
Referencia:
GA-861878
Investigador principal:
Andrés Hidalgo Alonso
Fecha inicio:
01/01/2020
Fecha fin:
31/12/2024
Presupuesto concedido:
400.000,00 €
Fuente de financiación:
EC-European Commission
Título:
Personalized Prevention for Coronary Heart Disease
Acrónimo
CoroPrevention
Convocatoria:
H2020-SC1-BHC-25-2019
Referencia:
GA-848056
Investigador principal:
Borja Ibáñez Cabeza
Fecha inicio:
01/01/2020
Fecha fin:
31/12/2026
Presupuesto concedido:
228.750,00 €
Fuente de financiación:
EC-European Commission
Título:
EXpansion and Phenotype Loss Of SMCs In Atherosclerosis: Causal effects and therapeutic possibilities
Acrónimo
EXPLOSIA
Convocatoria:
H2020-ERC-2019-COG
Referencia:
GA-866240
Investigador principal:
Jacob Fog Bentzon
Fecha inicio:
01/08/2020
Fecha fin:
31/07/2025
Presupuesto concedido:
702.755,00 €
Fuente de financiación:
EC-European Research Council
Título:
European Research Training in Understanding the Molecular Regulation and the Role of EndoLysosomal Processes in Cardio-Metabolic Diseases
Acrónimo
EndoConnect
Convocatoria:
H2020-MSCA-ITN-2020
Referencia:
953489
Investigador principal:
Miguel Ángel del Pozo Barriuso
Fecha inicio:
01/01/2021
Fecha fin:
31/12/2022
Fuente de financiación:
EC-European Commission
Título:
Machine learning artificial intelligence early detection stroke atrial fibrillation
Acrónimo
MAESTRIA
Convocatoria:
SC1-BHC-06-2020
Referencia:
GA-965286
Investigador principal:
José Jalife Sacal
Fecha inicio:
01/03/2021
Fecha fin:
28/02/2026
Presupuesto concedido:
801.000,00 €
Fuente de financiación:
EC-European Commission
Título:
Understanding and modulating vascular arrest with ultra-high definition
Acrónimo
AngioUnrestUHD
Convocatoria:
H2020-ERC-2020-COG
Referencia:
GA-101001814
Investigador principal:
Rui Benedito
Fecha inicio:
01/03/2021
Fecha fin:
28/02/2026
Presupuesto concedido:
1.998.500,00 €
Fuente de financiación:
EC-European Research Council
Título:
Remote Ischemic Conditioning in Lymphoma Patients Receiving Anthracyclines
Acrónimo
RESILIENCE
Convocatoria:
SC1-BHC-08-2020
Referencia:
GA-945118
Investigador principal:
Borja Ibáñez Cabeza
Fecha inicio:
01/06/2021
Fecha fin:
31/05/2026
Presupuesto concedido:
1.725.938,00 €
Fuente de financiación:
EC-European Commission
Resumen:
RESILIENCE: a European Commission-funded project, coordinated by CNIC, aimed at reducing the incidence of heart failure in cancer survivors Cancer survivors are at high risk for cardiovascular complications. Anthracyclines are an extremely effective treatment against many cancer types, but they can induce cardiac toxicity resulting in chronic heart failure. RESILIENCE will test a novel preventive intervention (remote ischemic conditioning) in patients at risk for anthracycline-induced cardiotoxicity. In addition, new diagnostic modalities will be used to identify anthracyclines-induced cardiotoxicity in its very early stages. RESILIENCE counts on a multidisciplinary consortium with the active participation of patients.
Enlace:
Título:
Rituximab in patients with acute myocardial infarction: a phase 2 placebo-controlled randomised clinical trial
Acrónimo
RITA ME 2
Convocatoria:
SC1-BHC-08-2020
Referencia:
GA-899991
Investigador principal:
Borja Ibáñez Cabeza
Fecha inicio:
01/06/2021
Fecha fin:
31/05/2026
Presupuesto concedido:
53.957,50 €
Fuente de financiación:
EC-European Commission
Título:
Uncovering Protein Mechanics in Physiology and Disease
Acrónimo
ProtMechanics-Live
Convocatoria:
H2020-ERC-2020-COG
Referencia:
GA-101002927
Investigador principal:
Jorge Alegre-Cebollada
Fecha inicio:
01/06/2021
Fecha fin:
31/05/2026
Presupuesto concedido:
2.000.000,00 €
Fuente de financiación:
EC-European Research Council
Título:
STING signalling modulation via the Electron Transport Chain
Acrónimo
STIMULATE
Convocatoria:
H2020-MSCA-IF-2019
Referencia:
GA-892965
Investigador principal:
Gillian Dunphy
Fecha inicio:
01/07/2021
Fecha fin:
30/06/2023
Presupuesto concedido:
160.932,48 €
Fuente de financiación:
EC-European Commission
Título:
Functional relevance of mitochondrial supercomplex assembly in myeloid cells
Acrónimo
MY MITOCOMPLEX
Convocatoria:
H2020-MSCA-IF-2019
Referencia:
GA-893682
Investigador principal:
Dieke Van Dinther
Fecha inicio:
01/11/2021
Fecha fin:
31/10/2023
Presupuesto concedido:
172.932,48 €
Fuente de financiación:
EC-European Commission
Título:
DecIphering nucLEar Mechanics in diabetes: a Multi-scAle perspective
Acrónimo
DILEMMA
Convocatoria:
HORIZON-MSCA-Postdoctoral Fellowships 2021
Referencia:
101065552
Investigador principal:
Andra C. Dumitru
Fecha inicio:
01/06/2022
Fecha fin:
14/12/2022
Presupuesto concedido:
181.152,96 €
Fuente de financiación:
EC-European Commission