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CVD in RA SIGNED

Mechanistic links between rheumatoid arthritis and cardiovascular complications: investigation on inflammation induced alterations in induced pluripotent stem cell-derived cardiomyocytes

Total Cost €

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EC-Contrib. €

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Partnership

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Project "CVD in RA" data sheet

The following table provides information about the project.

Coordinator
SLASKI PARK TECHNOLOGII MEDYCZNYCH KARDIO-MED SILESIA SPOLKA Z OGRANICZONA ODPOWIEDZIALNOSCIA 

Organization address
address: MARII CURIE SKLODOWSKIEJ 10C
city: ZABRZE
postcode: 41800
website: n.a.

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Poland [PL]
 Total cost 149˙625 €
 EC max contribution 149˙625 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2020
 Duration (year-month-day) from 2020-04-01   to  2022-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    SLASKI PARK TECHNOLOGII MEDYCZNYCH KARDIO-MED SILESIA SPOLKA Z OGRANICZONA ODPOWIEDZIALNOSCIA PL (ZABRZE) coordinator 149˙625.00

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 Project objective

The aim of this project is to uncover the mechanisms by which patients with rheumatoid arthritis (RA) may have an elevated risk of cardiovascular complications. In particular, we will determine the role of the inflamed joint microenvironment in promoting cellular bioenergetics of cardiomyocytes. We aim to test the hypothesis that cardiomyocytes of RA patients reflect the features of pathological changes that might indicate for the cardiac vulnerability characteristic for this disease. This proposal has three specific objectives: (1) To examine whether exposure of control and RA-specific induced pluripotent stem cells-derived cardiomyocytes (RA-iPSC-CMs) into a joint-like environment recapitulate a cardiac disease-like state; (2) to determine the effect of a joint-like environment on cellular bioenergetics of control and RA-iPSC-derived CMs; and (3) to test whether control and RA-iPSC-CMs can act as a tool to identify potential cardioprotective/cardiotoxic treatment strategies used in RA.

This project proposes a truly translational, bench-to-bedside approach building on the strength of the human RA model. We will establish a unique source of functional cardiomyocytes by reprogramming RA synovial fibroblasts and peripheral blood mononuclear cells to iPSC. To investigate the impact of the joint inflammation on cardiomyocytes’ bioenergetics and transcriptomic profile, the state-of-the-art technologies will be applied. The most advanced cell metabolism analyser will be used to quantify real-time measurements of mitochondrial respiration and glycolysis. Global analysis of mRNA and miRNA transcriptome by RNA-seq will allow identifying new cardiomyocyte-specific genes/pathways that might affect cellular metabolism in RA.

Using iPSC-CMs will provide a unique opportunity to examine the pathophysiology of cardiac involvement in RA and to evaluate whether they may serve as a preclinical platform for precision medicine.

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The information about "CVD IN RA" are provided by the European Opendata Portal: CORDIS opendata.

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