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RAMBO SIGNED

Mitochondrial DNA degradation and sterile inflammation in the heart

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 RAMBO project word cloud

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

therapeutic    mtdna    vivo    fuse    treat    cardiac    treatment    isoform    dysregulated    free    synthesis    mediated    genesis    pilot    removed    subcellular    therapeutics    mortality    cells    functional    nat    mechanism    inflammatory    components    energy    elucidated    cardiomyocytes    13    escapes    homologue    hearts    motifs    induces    damaged    generation    examine    functions    failing    inflammatogenic    bcl2    fragmentation    dynamic    2012    function    divide    radicals    significance    attempt    divides    countries    mitochondrial    mitochondria    reported    medicated    protein    nuclear    efficient    organelles    2007    mammalian    press    selectively    leads    nature    methylation    elucidate    contains    epigenetic    quality    mammals    cellular    yeast    dna    unmethylated    heart    showed    transcription    regulation    commun    physiological    methyltransferase    mitophagy    med    patient    selective    atg32    fission    elongated    autophagy    inflammation    normal    morbidity    bacteria    degradation    cpg    pieces    damage    preceded   

Project "RAMBO" data sheet

The following table provides information about the project.

Coordinator
KING'S COLLEGE LONDON 

Organization address
address: STRAND
city: LONDON
postcode: WC2R 2LS
website: www.kcl.ac.uk

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 United Kingdom [UK]
 Project website https://sites.google.com/view/ramboerc/home
 Total cost 2˙499˙817 €
 EC max contribution 2˙499˙817 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2015-AdG
 Funding Scheme ERC-ADG
 Starting year 2016
 Duration (year-month-day) from 2016-09-01   to  2021-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON UK (LONDON) coordinator 2˙499˙817.00

Map

 Project objective

Heart failure is the leading cause of morbidity and mortality in developed countries including EU. Novel and efficient therapeutics to treat patient with heart failure have to be developed. Mitochondria are subcellular organelles that produce energy and dynamic organelles that fuse and divide. Dysregulated mitochondrial activity results in generation of free radicals which cause damage to cellular components. We reported that mitochondrial quality control by autophagy is essential for normal cardiac functions (Nat Med 2007). Mitochondrial DNA (mtDNA) contains bacteria-like unmethylated CpG motifs, which are inflammatogenic. We reported that mtDNA that escapes from autophagy-mediated degradation leads to inflammatory responses in cardiomyocytes and heart failure (Nature 2012). Damaged mitochondria in failing hearts are selectively removed by mitochondria-selective autophagy, mitophagy. Mitophagy is preceded by mitochondrial fission, which divides elongated mitochondria into pieces for autophagy. Although Atg32 is essential for mitophagy in yeast, no homologue has been known in mammals. Recently, we identified Bcl2-like protein 13 (Bcl2-L-13) as a functional mammalian homologue of Atg32 which induces mitochondrial fragmentation and mitophagy (Nat Commun in press) in mammalian cells. While methylation of nuclear DNA involves in epigenetic regulation of protein synthesis, the significance of mtDNA methylation in transcription and autophagy-medicated inflammation remains to be elucidated. Our pilot study showed an isoform of DNA methyltransferase targets to mitochondria for mtDNA methylation. In this proposal, we shall attempt to characterize regulation mechanism of Bcl2-L-13 and its in vivo function and to elucidate the physiological significance of mtDNA methylation. Furthermore, we shall elucidate the role of mtDNA methylation and Bcl2-L-13 in the genesis of heart failure and examine whether these will be the therapeutic targets for the treatment of heart failure.

 Publications

year authors and title journal last update
List of publications.
2019 Tomokazu Murakawa, Koji Okamoto, Shigemiki Omiya, Manabu Taneike, Osamu Yamaguchi, Kinya Otsu
A Mammalian Mitophagy Receptor, Bcl2-L-13, Recruits the ULK1 Complex to Induce Mitophagy
published pages: 338-345.e6, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2018.12.050
Cell Reports 26/2 2019-07-25

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