Project: POCI-01-0145-FEDER-016385

Project name:	New Targets in DIAstolic heart failure: from coMOrbidities to persoNalizeD medicine
Project code:	POCI-01-0145-FEDER-016385
Main Objective:	Reforçar a investigação, o desenvolvimento tecnológico e a inovação
Intervention Region:	Norte
Proposing institution/Lead promoter/Coordinating entity:	Faculdade de Medicina da Universidade do Porto
Partner(s)/Co-promoter(s)/Participating institution(s):	Faculdade de Ciências Médicas; IBMC - Instituto de Biologia Molecular e Celular ; Instituto de Biologia Experimental e Tecnológica; Instituto Nacional de Engenharia Biomédica; IPATIMUP - Instituto de Patologia e Imunologia Molecular da UP; Universidade de Aveiro
Date of approval:	2016-09-30
Start date:	2016-12-01
Completion date:	2021-02-28

Total Financial Support

União Europeia - FEDER:

578.823,83 EUR

Objectives, activities and expected/achieved results

Objetivos e Atividades
NETDIAMOND joins a network of national centres of reference with complementary expertizes to address this novel and highly relevant issue: to unravel key routes and mechanisms that lead from comorbidities to endothelial dysfunction, disturbed mechanisms of intercellular communication and ultimately to cardiomyocyte dysfunction in HFpEF. Thus NETDIAMOND has the following objectives:
1. implement a national multicentric standard practise of clinical, functional and follow-up data, and myocardial sample collection in HFpEF patients as well as a national registry for HFpEF;
2. examine well-characterized cohorts of HFpEF patients and their blood sample banks by comprehensive high throughput omics approaches, from genome to proteome, and apply omics approaches in paired samples of tissues such as myocardium and adipose tissue from patients with or without certain comorbidities as a step towards precision medicine;

Resultados Esperados/Atingidos
NETDIAMOND's main topic of research, HFpEF, is a major current health issue. The role of underlying comorbidities as drivers of disease progression by way of inflammation and microvascular dysfunction remains undefined. NETDIAMOND addresses this issue with state-of-the-art methodologies and complementary strategies from a discovery science approach based on omics that will identify gene variants that may predispose to disease and gene and protein expression profiles related to each of the major comorbidities. This will enable a systems biology view of HFpEF by advanced mathematical modelling, to a hypothesis-driven research of the mechanisms of disturbed cell communication and cellular dysfunction in endothelial cells, adipocytes, cardiac fibroblasts, inflammatory cells and cardiomyocytes that lead from systemic inflammation to microvascular dysfunction and ultimately cardiomyocyte stiffness. These mechanisms will be investigated by cellular culture and co-culture and in vitro

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