Grant: Master's Award: Canada Graduate Scholarships
York University (Toronto, Ontario)
$17,500.00
Determining the efficacy of a novel antioxidant targeting mitochondrial bioenergetics in preventing muscle degradation in muscular dystrophies
EF 2013-14
Résumé
Muscle wasting is a condition present is a wide variety of populations ranging from aging individuals to those affected by muscular dystrophies. It is the leading cause of morbidity and mortality as it restricts the ability to move, circulate blood and even breathe. Despite its severity and prevalence, there is currently no cure for the condition. One of the key components associated with muscle wasting is elevated reactive oxygen species (ROS) production, a byproduct of energy production controlled by the mitochondria. Consequently, many attempts at the use of antioxidants to decrease the oxidative stress that results from a ROS overload have been made. Unfortunately, the specific pathway of ROS production that needs to be targeted remains unknown and as a result, many of these antioxidants have been unsuccessful. The proposed research involves the use of a mitochondria specific antioxidant in an attempt to counteract oxidative stress based on the recent findings that mitochondrial ROS production specifically is increased during muscle wasting. The efficacy of this antioxidant will be tested using mdx mice, a model of Duchenne Muscular Dystrophy, the most common and severe form of muscular dystrophy seen in 1 in 3000 boys. The extent of muscle wasting in mdx mice receiving the novel antioxidant will be monitored in comparison to their mdx control counterparts. The findings from this study will help to determine is mitochondrial ROS are indeed causal for triggering the muscle wasting seen in this model of muscular dystrophy.
Programme
Master's Award: Canada Graduate Scholarships
Bénéficiaire
Emplacement
Ontario, Canada
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
311871
Name
Hughes Meghan C
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Prcname2
Special Cases - Awards Programs
Projecttitle
Determining the efficacy of a novel antioxidant targeting mitochondrial bioenergetics in preventing muscle degradation in muscular dystrophies
Programtype2
Studentship Programs
Orgnameinp2
York University (Toronto, Ontario)
Cihramount2
$17,500
Cihrequipment2
$0
Programname2
Master's Award: Canada Graduate Scholarships
Keyworddelim
Antioxidants; Bioenergetics; Cell Regulation; Degeneration; Mitochondria; Muscle Metabolism; Muscle Wasting; Pathway Regulation; Reactive Oxygen Species; Redox
Abstract
Muscle wasting is a condition present is a wide variety of populations ranging from aging individuals to those affected by muscular dystrophies. It is the leading cause of morbidity and mortality as it restricts the ability to move, circulate blood and even breathe. Despite its severity and prevalence, there is currently no cure for the condition. One of the key components associated with muscle wasting is elevated reactive oxygen species (ROS) production, a byproduct of energy production controlled by the mitochondria. Consequently, many attempts at the use of antioxidants to decrease the oxidative stress that results from a ROS overload have been made. Unfortunately, the specific pathway of ROS production that needs to be targeted remains unknown and as a result, many of these antioxidants have been unsuccessful. The proposed research involves the use of a mitochondria specific antioxidant in an attempt to counteract oxidative stress based on the recent findings that mitochondrial ROS production specifically is increased during muscle wasting. The efficacy of this antioxidant will be tested using mdx mice, a model of Duchenne Muscular Dystrophy, the most common and severe form of muscular dystrophy seen in 1 in 3000 boys. The extent of muscle wasting in mdx mice receiving the novel antioxidant will be monitored in comparison to their mdx control counterparts. The findings from this study will help to determine is mitochondrial ROS are indeed causal for triggering the muscle wasting seen in this model of muscular dystrophy.
Competitiondate
201312
Approvedterm2
1 yr 0 mth
Pinamesdelim
Hughes, Meghan C
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $17,500~ $0~