Grant: Project Grant
University of Alberta
$100,000.00
Improving Mitochondria in Aged Hearts Following Ischemia-Reperfusion Injury with Novel Epoxy Lipids
EF 2016-17
Résumé
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in elderly individuals, where they can make up an estimated 75% of patients presenting with coronary artery disease or heart failure. Ischemic heart disease is one category that accounts for a significant portion of all CVD. Heart damage begins to occur after it has been deprived of oxygen (ischemia) for an extended period of time. The immediate return of blood flow (reperfusion) to the heart is important. While mortality rates have decreased over the last 30 years, myocardial ischemic injury remains a critical problem. Survival after a heart attack often leads to individuals living with significantly damaged hearts, with over 30-40% of heart attack survivors progressing to heart failure. Determining the pathological progression is made more difficult by the multiple changes to cardiovascular structure and function that occur during normal ageing. In the heart, mitochondria provide about 90% of the energy for cardiac function. It has been shown that deterioration of mitochondria over time plays a critical role in age-related cardiac dysfunction. Therefore, maintenance of a healthy mitochondrial population is essential for the preservation of healthy cardiac muscle. The overall goal of this project is to investigate the cardioprotective effects of novel metabolites produced from omega-3 fatty acids. Proteins within a cell metabolize these omega-3 fatty acids into active molecules called epoxy lipids. These molecules are involved in regulating different functions in the body. Our research has demonstrated they can limit mitochondrial injury. Thus, the objective of the grant is to investigate how this occurs in young versus aged hearts. We will investigate if these molecules are viable therapeutic strategies to prevent and/or treat mitochondrial damage caused by ischemia-reperfusion injury. We aim to identify new regulatory mechanisms and advance our understanding of mitochondrial function.
Programme
Project Grant
Bénéficiaire
Emplacement
Alberta, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
366580
Name
Seubert John M
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Project Grant Competition
Projecttitle
Improving Mitochondria in Aged Hearts Following Ischemia-Reperfusion Injury with Novel Epoxy Lipids
Programtype2
Operating Grants
Orgnameinp2
University of Alberta
Cihramount2
$100,000
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Ageing; Cardiac; Cytochrome P450 Epoxygenases; Drug Development; Eicosanoids; Human Explanted Heart; Ischemia/Reperfusion Injury; Mitochondria; Omega-3 Pufa; Soluble Epoxide Hydrolase
Abstract
Cardiovascular disease (CVD) is a leading cause of morbidity and mortality in elderly individuals, where they can make up an estimated 75% of patients presenting with coronary artery disease or heart failure. Ischemic heart disease is one category that accounts for a significant portion of all CVD. Heart damage begins to occur after it has been deprived of oxygen (ischemia) for an extended period of time. The immediate return of blood flow (reperfusion) to the heart is important. While mortality rates have decreased over the last 30 years, myocardial ischemic injury remains a critical problem. Survival after a heart attack often leads to individuals living with significantly damaged hearts, with over 30-40% of heart attack survivors progressing to heart failure. Determining the pathological progression is made more difficult by the multiple changes to cardiovascular structure and function that occur during normal ageing. In the heart, mitochondria provide about 90% of the energy for cardiac function. It has been shown that deterioration of mitochondria over time plays a critical role in age-related cardiac dysfunction. Therefore, maintenance of a healthy mitochondrial population is essential for the preservation of healthy cardiac muscle. The overall goal of this project is to investigate the cardioprotective effects of novel metabolites produced from omega-3 fatty acids. Proteins within a cell metabolize these omega-3 fatty acids into active molecules called epoxy lipids. These molecules are involved in regulating different functions in the body. Our research has demonstrated they can limit mitochondrial injury. Thus, the objective of the grant is to investigate how this occurs in young versus aged hearts. We will investigate if these molecules are viable therapeutic strategies to prevent and/or treat mitochondrial damage caused by ischemia-reperfusion injury. We aim to identify new regulatory mechanisms and advance our understanding of mitochondrial function.
Competitiondate
201611
Approvedterm2
1 yr 0 mth
Pinamesdelim
Seubert, John M
Approvedterm
1 an 0 mois
Cihrcontribution2
~ $100,000~ $0~