New therapeutic targets in valve and myocardial alterations associated with the development and progression of aortic stenosis: pathophysiology and Therapeutic Innovation. (Q3155365): Difference between revisions

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(‎Changed label, description and/or aliases in en: translated_label)
(‎Removed claim: summary (P836): Severe degenerative aortic stenosis (SD) is a very prevalent disease, the incidence of which will increase in the coming years due to population ageing. There is currently no pharmacological treatment that slows its progression, and when symptoms appear, valve replacement surgery, which can be performed open or percutaneously (TAVI), is the only treatment. EA is characterised by calcification of the aortic valve and the appearance of myocardia...)
Property / summary
Severe degenerative aortic stenosis (SD) is a very prevalent disease, the incidence of which will increase in the coming years due to population ageing. There is currently no pharmacological treatment that slows its progression, and when symptoms appear, valve replacement surgery, which can be performed open or percutaneously (TAVI), is the only treatment. EA is characterised by calcification of the aortic valve and the appearance of myocardial fibrosis. However, the pathophysiological mechanisms of EA necessary to identify and develop new appropriate therapeutic strategies are not known. Galectin-3 (Gal-3) is a mediator of cardiac fibrosis, and regulates osteogenesis in atherosclerosis, being its beneficial inhibition. The objective of this study is to analyse whether Gal-3 can be a new therapeutic target in valvular calcification and myocardial fibrosis associated with progression of EA. In addition, Gal-3 could be a biomarker identifying patients who would benefit from early valve replacement. Our main objectives will be: 1) Study the mechanisms that Gal-3 uses to induce valvular calcification and myocardial fibrosis using cell models. 2) Analyse whether Gal-3 inhibition could improve EA-related alterations in animal models. 3) Analyse whether Gal-3 is a biomarker of EA progression and whether it can be used for stratification of patients who would benefit from early surgery and therefore personalised medicine. This project will lead to the validation of a new therapeutic target, allowing better understanding of the pathophysiology of the EA and improving the options for individualising the treatment of EA. (English)
 
Property / summary: Severe degenerative aortic stenosis (SD) is a very prevalent disease, the incidence of which will increase in the coming years due to population ageing. There is currently no pharmacological treatment that slows its progression, and when symptoms appear, valve replacement surgery, which can be performed open or percutaneously (TAVI), is the only treatment. EA is characterised by calcification of the aortic valve and the appearance of myocardial fibrosis. However, the pathophysiological mechanisms of EA necessary to identify and develop new appropriate therapeutic strategies are not known. Galectin-3 (Gal-3) is a mediator of cardiac fibrosis, and regulates osteogenesis in atherosclerosis, being its beneficial inhibition. The objective of this study is to analyse whether Gal-3 can be a new therapeutic target in valvular calcification and myocardial fibrosis associated with progression of EA. In addition, Gal-3 could be a biomarker identifying patients who would benefit from early valve replacement. Our main objectives will be: 1) Study the mechanisms that Gal-3 uses to induce valvular calcification and myocardial fibrosis using cell models. 2) Analyse whether Gal-3 inhibition could improve EA-related alterations in animal models. 3) Analyse whether Gal-3 is a biomarker of EA progression and whether it can be used for stratification of patients who would benefit from early surgery and therefore personalised medicine. This project will lead to the validation of a new therapeutic target, allowing better understanding of the pathophysiology of the EA and improving the options for individualising the treatment of EA. (English) / rank
Normal rank
 
Property / summary: Severe degenerative aortic stenosis (SD) is a very prevalent disease, the incidence of which will increase in the coming years due to population ageing. There is currently no pharmacological treatment that slows its progression, and when symptoms appear, valve replacement surgery, which can be performed open or percutaneously (TAVI), is the only treatment. EA is characterised by calcification of the aortic valve and the appearance of myocardial fibrosis. However, the pathophysiological mechanisms of EA necessary to identify and develop new appropriate therapeutic strategies are not known. Galectin-3 (Gal-3) is a mediator of cardiac fibrosis, and regulates osteogenesis in atherosclerosis, being its beneficial inhibition. The objective of this study is to analyse whether Gal-3 can be a new therapeutic target in valvular calcification and myocardial fibrosis associated with progression of EA. In addition, Gal-3 could be a biomarker identifying patients who would benefit from early valve replacement. Our main objectives will be: 1) Study the mechanisms that Gal-3 uses to induce valvular calcification and myocardial fibrosis using cell models. 2) Analyse whether Gal-3 inhibition could improve EA-related alterations in animal models. 3) Analyse whether Gal-3 is a biomarker of EA progression and whether it can be used for stratification of patients who would benefit from early surgery and therefore personalised medicine. This project will lead to the validation of a new therapeutic target, allowing better understanding of the pathophysiology of the EA and improving the options for individualising the treatment of EA. (English) / qualifier
point in time: 12 October 2021
Timestamp+2021-10-12T00:00:00Z
Timezone+00:00
CalendarGregorian
Precision1 day
Before0
After0
 

Revision as of 15:49, 12 October 2021

Project Q3155365 in Spain
Language Label Description Also known as
English
New therapeutic targets in valve and myocardial alterations associated with the development and progression of aortic stenosis: pathophysiology and Therapeutic Innovation.
Project Q3155365 in Spain

    Statements

    contained in NUTS
    Navarre
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    country
    Spain
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    EU contribution
    50,750.0 Euro
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    budget
    101,500.0 Euro
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    co-financing rate
    50.0 percent
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    start time
    1 January 2016
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    end time
    31 August 2019
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    beneficiary name (string)
    FUNDACION INSTITUTO DE INVESTIGACION SANITARIA DE NAVARRA
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    beneficiary
    Q3137938
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    coordinate location

    42°49'6.42"N, 1°38'39.34"W
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    postal code
    31201
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    summary
    La estenosis aórtica severa degenerativa (EA) es una enfermedad muy prevalente, cuya incidencia se incrementará en los próximos años debido al envejecimiento de la población. Actualmente no existe ningún tratamiento farmacológico que retarde su progresión, y cuando aparecen los síntomas, la cirugía de recambio valvular, que puede realizarse a corazón abierto o de forma percutánea (TAVI), es el único tratamiento. La EA se caracteriza por la calcificación de la válvula aórtica y por la aparición de fibrosis miocárdica. Sin embargo, no se conocen los mecanismos fisiopatológicos de la EA necesarios para identificar y desarrollar nuevas estrategias terapéuticas adecuadas. La Galectina-3 (Gal-3) es un mediador de fibrosis cardíaca, y regula la osteogénesis en la aterosclerosis, siendo su inhibición beneficiosa. El objetivo de este estudio es analizar si la Gal-3 puede ser una nueva diana terapéutica en la calcificación valvular y la fibrosis miocárdica asociadas a la progresión de la EA. Además, la Gal-3 podría ser un biomarcador que identificara a los pacientes que se beneficiarían de un recambio valvular precoz. Nuestros objetivos principales serán: 1) Estudiar los mecanismos que utiliza la Gal-3 para inducir calcificación valvular y fibrosis miocárdica usando modelos celulares. 2) Analizar si la inhibición de Gal-3 podría mejorar las alteraciones asociadas a la EA en modelos animales. 3) Analizar si la Gal-3 es un biomarcador de la progresión de la EA y si puede ser usado para la estratificación de pacientes que se beneficiarían de una cirugía precoz y por tanto de una medicina personalizada. Este proyecto llevará a la validación de una nueva diana terapéutica, permitiendo conocer mejor la fisiopatología de la EA y mejorando las opciones para individualizar el tratamiento de la EA. (Spanish)
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    location (string)
    Pamplona/Iruña
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    Identifiers

    Spanish Kohesio ID
    PI15_02160
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