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MITOPOMPE SIGNED

Targeting mitochondrial defects and oxidative stress in Pompe Disease: from pathogenesis to therapy

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 MITOPOMPE project word cloud

Explore the words cloud of the MITOPOMPE project. It provides you a very rough idea of what is the project "MITOPOMPE" about.

calcium    mutations    cell    phosphorylation    rescue    cardiomyopathy    gaa    cellular    pathophysiology    neuromuscular    group    lsds    dependent    competent    pathology    reversal    functional    function    disease    apoptosis    extensive    acid    therapeutic    therapy    severity    interacting    boost    accordingly    pompe    tissues    model    treatment    synapses    dr    potentially    phenotypes    active    avenues    mitochondria    nervous    antioxidants    expertise    mingozzi    buffering    neuron    caused    treat    muscle    enzyme    evident    combined    signaling    regulated    dysfunction    atp    disorders    ko    organelle    glucosidase    transmission    stress    alpha    weakness    heavily    depending    aav    gene    pd    full    neuronal    pharmaceutical    lsd    transcriptomic    mitoq    interventions    defects    therapies    fighting    sequencing    central    mtgsh    point    involvement    amounts    everyday    mouse    respiratory    little    lysosomal    mitochondrial    brain    muscular    tested    perform    storage    functionally    rna    oxidative    nrf2    motor    mitocatalase    missing    complemented    synaptic    neurological   

Project "MITOPOMPE" data sheet

The following table provides information about the project.

Coordinator
ASSOCIATION GENETHON 

Organization address
address: RUE DE L INTERNATIONALE 1 BIS
city: EVRY
postcode: 91002
website: www.genethon.fr

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 France [FR]
 Total cost 173˙076 €
 EC max contribution 173˙076 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2017
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2019
 Duration (year-month-day) from 2019-01-01   to  2020-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    ASSOCIATION GENETHON FR (EVRY) coordinator 173˙076.00

Map

 Project objective

The central role of ATP production by oxidative-phosphorylation, together with calcium buffering and apoptosis, makes mitochondria an organelle interacting with many processes within the cell. Neuronal and muscular tissues require high amounts of ATP to perform their everyday function, therefore are heavily dependent on mitochondrial function. Neuromuscular synapses are of particular importance since synaptic transmission is a highly regulated process which requires active and functionally competent mitochondria. Accordingly, mitochondrial involvement is becoming increasingly evident in is Lysosomal Storage Disorders (LSDs) along with neurological pathology. Over the past several years Dr. Mingozzi’s group has built extensive expertise in Pompe Disease (PD), an LSD which is caused by mutations in the enzyme acid α-glucosidase (GAA). Muscle weakness, cardiomyopathy, respiratory failure, central nervous system and more specifically motor-neuron defects are observed depending on the severity of the disease. Little is known about the role of mitochondria in the pathophysiology of PD and interventions aimed at addressing mitochondrial defects in PD is currently missing. The aim of this proposal is to characterize the mitochondrial dysfunction in the Gaa KO mouse model of PD. This to assess potential rescue of such phenotypes by AAV-based GAA gene therapy complemented with therapeutic interventions targeted to treat and boost mitochondrial function by fighting against oxidative stress. Two mitochondrial treatment approaches; (i) pharmaceutical antioxidants, e.g. mitoQ or mtGSH and (ii) AAV based approaches; AAV-Nrf2 and AAV-mitoCatalase will be tested. Combined therapies with the AAV-GAA treatment will aim to reach full rescue of the muscle and brain pathology and functional reversal of mitochondrial defects. Transcriptomic changes will also be analyzed by RNA sequencing to investigate cellular signaling changes which will potentially point to novel therapeutic avenues.

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The information about "MITOPOMPE" are provided by the European Opendata Portal: CORDIS opendata.

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