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Grant: Project Grant

University of Ottawa

$722,926.00

Mitochondrial dynamics and metabolism in muscle stem cell maintenance and muscle regeneration

EF 2019-20

Résumé
An estimated 4 million Canadians currently suffer from muscle wasting conditions, manifesting as loss of muscle mass and function. Muscle wasting is the most significant cause of disability in the aging population and individuals with muscle degenerative diseases, including muscular dystrophies, myopathies and cancer cachexia. The decline in muscle function affects mobility, voluntary function and quality of life, often leading to institutionalization and mortality4. This imposes a dramatic burden on individuals and society, costing Canadians several billions of dollars per year. Thus, there is a pressing need for the development of preventative and therapeutic strategies targeting muscle wasting. For many years, muscle wasting was thought to be only a problem of the myofibers, yet recent evidence shows that muscle stem cell (MuSC) dysfunction plays a significant role. Adult skeletal muscle normally has a high regenerative capacity, however, within the context of muscle wasting MuSCs are depleted and muscle regeneration is impaired. Currently, the reason for MuSC depletion is unclear and thus there are no therapies targeting their restoration. Understanding the underlying etiological factors leading to MuSC depletion is instrumental in identifying novel approaches to restore muscle repair and function. The overarching goal of this proposal is to restore MuSC number and function and promote muscle repair in aging and muscle wasting diseases.
Programme
Project Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
421341
Name
Khacho Mireille
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Musculoskeletal Health and Arthritis
Theme2
Biomedical
Prcname2
Movement & Exercise
Projecttitle
Mitochondrial dynamics and metabolism in muscle stem cell maintenance and muscle regeneration
Programtype2
Operating Grants
Orgnameinp2
University of Ottawa
Cihramount2
$722,926
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Glutathione; Mitochondrial Fission And Fusion; Mitochondrial Function And Metabolism; Muscle Atrophy; Muscle Function; Muscle Regeneration; Muscle Stem Cell Maintenance; Myopathies, Muscle Degenerative Diseases And Aging; Reactive Oxygen Species
Abstract
An estimated 4 million Canadians currently suffer from muscle wasting conditions, manifesting as loss of muscle mass and function. Muscle wasting is the most significant cause of disability in the aging population and individuals with muscle degenerative diseases, including muscular dystrophies, myopathies and cancer cachexia. The decline in muscle function affects mobility, voluntary function and quality of life, often leading to institutionalization and mortality4. This imposes a dramatic burden on individuals and society, costing Canadians several billions of dollars per year. Thus, there is a pressing need for the development of preventative and therapeutic strategies targeting muscle wasting. For many years, muscle wasting was thought to be only a problem of the myofibers, yet recent evidence shows that muscle stem cell (MuSC) dysfunction plays a significant role. Adult skeletal muscle normally has a high regenerative capacity, however, within the context of muscle wasting MuSCs are depleted and muscle regeneration is impaired. Currently, the reason for MuSC depletion is unclear and thus there are no therapies targeting their restoration. Understanding the underlying etiological factors leading to MuSC depletion is instrumental in identifying novel approaches to restore muscle repair and function. The overarching goal of this proposal is to restore MuSC number and function and promote muscle repair in aging and muscle wasting diseases.
Competitiondate
202003
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Khacho, Mireille
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $722,926~ $0~