Cel Hypertension is a common disease impacting 1 billion people worldwide, which leads to catastrophic cardiovascular complications. The cause of primary hypertension is unknown and the disease remains uncontrolled in many patients. By interrogating the key hypothesis that inflammatory dysregulation fundamentally controls development of hypertension and vascular remodelling, InflammaTENSION provides a new paradigm for the management of the disease, with the potential to lead to identification of novel therapeutic targets to control hypertension. InflammaTENSION will result in the discovery of novel biomarkers, capable of identifying patients who could benefit from such immune targeted therapies. Importantly, we already made the seminal observation that the immune system not only mediates target organ damage, but is essential for the development of hypertension. This finding has initiated numerous studies, that defined the roles of pro-inflammatory T cells, monocytes and anti-inflammatory T regulatory cells. However, our current knowledge remains very fragmented and so far has not been applied to human pathology. InflammaTENSION will for the first time advance the knowledge procured in rodent models into human studies. By combining clinical translational and model mechanistic studies it will identify novel inflammatory factors that can control immune mechanisms of hypertension. We will: (1) characterize the immunophenotypic signature of human hypertension; (2) define key concepts in cytokine biology of hypertension with TNF-α and IL-6 as key exemplars; (3) understand how chronic cytokines regulate the T cell dependent mechanisms of hypertension. InflammaTENSION will go beyond current state-of-the-art through comprehensive combination of immunology and cardiovascular medicine to create a new understanding of how the immune system may lead to human hypertension and will have major impact on the field, enabling translation of these exciting findings to clinical practice. Dziedzina nauki medical and health sciencesbasic medicineimmunologymedical and health sciencesbasic medicinepathology Słowa kluczowe hypertension blood pressure endothelium inflammation vascular perivascular Program(-y) H2020-EU.1.1. - EXCELLENT SCIENCE - European Research Council (ERC) Main Programme Temat(-y) ERC-2016-COG - ERC Consolidator Grant Zaproszenie do składania wniosków ERC-2016-COG Zobacz inne projekty w ramach tego zaproszenia System finansowania ERC-COG - Consolidator Grant Instytucja przyjmująca THE UNIVERSITY OF EDINBURGH Wkład UE netto € 165 243,75 Adres OLD COLLEGE, SOUTH BRIDGE EH8 9YL Edinburgh Zjednoczone Królestwo Zobacz na mapie Region Scotland Eastern Scotland Edinburgh Rodzaj działalności Higher or Secondary Education Establishments Linki Kontakt z organizacją Opens in new window Strona internetowa Opens in new window Uczestnictwo w unijnych programach w zakresie badań i innowacji Opens in new window sieć współpracy HORIZON Opens in new window Koszt całkowity € 165 243,75 Beneficjenci (2) Sortuj alfabetycznie Sortuj według wkładu UE netto Rozwiń wszystko Zwiń wszystko THE UNIVERSITY OF EDINBURGH Zjednoczone Królestwo Wkład UE netto € 165 243,75 Adres OLD COLLEGE, SOUTH BRIDGE EH8 9YL Edinburgh Zobacz na mapie Region Scotland Eastern Scotland Edinburgh Rodzaj działalności Higher or Secondary Education Establishments Linki Kontakt z organizacją Opens in new window Strona internetowa Opens in new window Uczestnictwo w unijnych programach w zakresie badań i innowacji Opens in new window sieć współpracy HORIZON Opens in new window Koszt całkowity € 165 243,75 UNIVERSITY OF GLASGOW Zjednoczone Królestwo Wkład UE netto € 1 792 330,00 Adres UNIVERSITY AVENUE G12 8QQ Glasgow Zobacz na mapie Region Scotland West Central Scotland Glasgow City Rodzaj działalności Higher or Secondary Education Establishments Linki Kontakt z organizacją Opens in new window Strona internetowa Opens in new window Uczestnictwo w unijnych programach w zakresie badań i innowacji Opens in new window sieć współpracy HORIZON Opens in new window Koszt całkowity € 1 792 330,00