REMAKIN SIGNED
REstoring myocardial repair capacity via the modulation of MAcrophage-mediated cytoKINe secretion.
Total Cost €
0EC-Contrib. €
0Partnership
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0REMAKIN project word cloud
Explore the words cloud of the REMAKIN project. It provides you a very rough idea of what is the project "REMAKIN" about.
Project "REMAKIN" data sheet
The following table provides information about the project.
| Coordinator |
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE
Organization address contact info |
| Coordinator Country | France [FR] |
| Total cost | 196˙707 € |
| EC max contribution | 196˙707 € (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 | 2019 |
| Duration (year-month-day) | from 2019-08-01 to 2021-07-31 |
Partnership
Take a look of project's partnership.
| # | ||||
|---|---|---|---|---|
| 1 | INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE | FR (PARIS) | coordinator | 196˙707.00 |
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Project objective
Type-2 diabetes (T2D) is a chronic condition strongly associated with cardiovascular diseases, mainly recurrent myocardial infarctions (MI), and generating enormous healthcare cost. Macrophages orchestrate the remodelling of the heart post-MI by efferocytosis-mediated cytokine secretion. Specifically, Mertk-mediated efferocytosis promotes vessel formation, tissue reperfusion and resolution of the inflammatory response via the secretion of the anti-inflammatory cytokines interleukin-10 (IL-10) and Vascular Endothelial Growth Factor-A (VEGF-A). In IR/T2D, efferocytosis-mediated cytokine secretion is impaired, leading to chronic inflammation, adverse post-MI remodelling, recurrent heart failure and excessive mortality. To date, the signalling and intracellular trafficking pathways leading to cytokines secretion are unknown, and the mechanisms of impairment during IR/T2D are unexplored. Previous therapeutic strategies focussed on repairing damaged tissue by injection of progenitor cells or modulating inflammation by cytokine injection, but both strategies gave disappointing results. In this proposal, I will define the mechanisms of efferocytosis-mediated cytokine secretion in macrophages, investigate their defects in IR/T2D and test a novel cell-based therapeutic strategy for improving recovery of T2D patients post-MI and preventing recurrence of cardiac events by restoring cytokine secretion in diabetic macrophages.
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The information about "REMAKIN" are provided by the European Opendata Portal: CORDIS opendata.