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Grant: Project Grant

University of Alberta

$970,785.00

Molecular mechanisms that promote cardiac cell survival and heart health

EF 2019-20

Résumé
In Canada, approximately 1.6 million people suffer from cardiovascular diseases, and someone dies from these diseases every 7 minutes. The heart is made of different cell types that work together to generate a heart beat. These cells share a common mechanism to handle cellular stress in response to unfavorable conditions, but the outcome of the stress coping strategy depends on the type of heart cell. A condition called cardiac fibrosis results from malfunction of the cell stress coping response, which eventually results in heart failure. We found that long-term stress coping response in cardiomyocytes, (the cells responsible for contraction and relaxation of the heart) and in cardiac fibroblasts (the cells responsible for repairing damage to heart tissue) is instrumental to development of cardiac fibrosis. On the other hand, we found that a drug called TUDCA is effective in preventing cardiac fibrosis in animal models. The proposed research aims to understand how the malfunction in cardiomyocyte and cardiac fibroblasts stress coping response mechanism promotes cardiac fibrosis, and how TUDCA prevents cardiac fibrosis. We will apply the new knowledge generated to guide therapeutic interventions that can prevent or treat the development of heart disease in humans.
Programme
Project Grant
Bénéficiaire
Emplacement
Alberta, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database

Tel que publié

Id
407862
Name
Michalak Marek S
Region
Alberta
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Circulatory and Respiratory Health
Theme2
Biomedical
Prcname2
Cardiovascular System - A: Cells and Tissues
Projecttitle
Molecular mechanisms that promote cardiac cell survival and heart health
Programtype2
Operating Grants
Orgnameinp2
University of Alberta
Cihramount2
$970,785
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Calcium Signaling; Endoplasmic Reticulum Stress; Fibrosis; Heart Failure; Molecular Chaperone; Proteostasis; Sarcoplasmic Reticulum; Stress Responses; Stress Sensor; Unfolded Protein Response
Abstract
In Canada, approximately 1.6 million people suffer from cardiovascular diseases, and someone dies from these diseases every 7 minutes. The heart is made of different cell types that work together to generate a heart beat. These cells share a common mechanism to handle cellular stress in response to unfavorable conditions, but the outcome of the stress coping strategy depends on the type of heart cell. A condition called cardiac fibrosis results from malfunction of the cell stress coping response, which eventually results in heart failure. We found that long-term stress coping response in cardiomyocytes, (the cells responsible for contraction and relaxation of the heart) and in cardiac fibroblasts (the cells responsible for repairing damage to heart tissue) is instrumental to development of cardiac fibrosis. On the other hand, we found that a drug called TUDCA is effective in preventing cardiac fibrosis in animal models. The proposed research aims to understand how the malfunction in cardiomyocyte and cardiac fibroblasts stress coping response mechanism promotes cardiac fibrosis, and how TUDCA prevents cardiac fibrosis. We will apply the new knowledge generated to guide therapeutic interventions that can prevent or treat the development of heart disease in humans.
Competitiondate
201909
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Michalak, Marek S; Agellon, Luis B
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $970,785~ $0~