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AtheroGLP1

Financiado

Unmasking the molecular mechanisms mediating the antiatherogenic effects of GLP-...

Unmasking the molecular mechanisms mediating the antiatherogenic effects of GLP-1RAs Cardiovascular diseases (CVD) are highly prevalent in Europe, causing more than 3.9 million deaths yearly. Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the main underlying cause of CVD. Available strat... ver más

31/08/2027

USC

253K€

Presupuesto del proyecto: 253K€

Líder del proyecto

UNIVERSIDAD DE SANTIAGO DE COMPOSTELA No se ha especificado una descripción o un objeto social para esta compañía.

Total investigadores 235

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Financiación concedida El organismo HORIZON EUROPE notifico la concesión del proyecto el día 2023-03-14

HORIZON-MSCA-2022-PF-01-01: MSCA Postdoctoral Fellowships 2022 ExpectedOutcome:

I+D

Cerrada hace 2 años

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2 Participantes

USC

252.72K€ | Lider

MSH

N.D. | Participante

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Duración del proyecto: 53 meses Fecha Inicio: 2023-03-14
Fecha Fin: 2027-08-31

Líder del proyecto

UNIVERSIDAD DE SANTIAGO DE COMPOSTELA No se ha especificado una descripción o un objeto social para esta compañía.

Total investigadores 235

Presupuesto del proyecto 253K€

Descripción del proyecto Cardiovascular diseases (CVD) are highly prevalent in Europe, causing more than 3.9 million deaths yearly. Atherosclerosis, a chronic inflammatory disease of the arterial wall, is the main underlying cause of CVD. Available strategies to treat and prevent atherosclerosis remain suboptimal, therefore, better understanding of its regulatory mechanisms is required to design new approaches to treat this inflammatory disease. Recent cardiovascular outcome trials demonstrated that GLP-1R agonists (GLP-1RA) reduce the rates of major cardiovascular events. This GLP-1RA effects are hypothesized to reflect modifications on atherosclerosis, through anti-inflammatory actions. However, the mechanisms linking GLP-1R activation to control of atherosclerosis and vascular inflammation, as well as the cells/tissues mediating these effects, are far from understood. The main aim of my proposal is to identify the mechanism by which GLP-1RA regulate atherosclerosis regression, offering a unique and innovative opportunity to study the role of yet unexplored GLP-1R+ cell types (vascular smooth muscle cells, and neurons of the enteric and central nervous system) mediating its effects. The multidisciplinary perspective adopted, combining my background in academic research with preclinical models, the experience in biomedical research of the host supervisor, and the clinic/translational perspective of the partner supervisor, gives this AtheroGLP1 project with the strong potential to identify novel mechanisms that are expected to have immediate translational importance for targeted use of GLP-1RAs in the clinic to treat atherosclerosis and CVD. Importantly, this proposal will allow me to gain transferable competences and get trained in the latest in vivo and molecular techniques to assess vascular and systemic inflammation, letting me to reach scientific maturity to stablish a similar facility at the host institution, promoting my transition to become an independent researcher in the ERA.

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