Grant: Project Grant
University of Toronto
$994,500.00
Investigating the role of NOD2 in intestinal fibrosis
EF 2023-24
Résumé
Intestinal fibrosis is a common debilitating complication associated with the inflammatorybowel disease (IBD), Crohn's disease (CD). There are no clinical solutions for preventing or treating fibrosis, except for surgical intervention. Therefore, there is a great unmet need to understand the mechanisms leading to fibrotic complications in CD. In general, fibrosis is a consequence of dysregulated healing processes. We have developed a mouse model of chronic intestinal inflammation where mice possess one of the gene variants associated with human CD develop fibrosis. Using this model, we can now determine how the process by which cells in the intestine promote fibrosis, which may reveal targetable pathways for the treatment or prevention of this severe complication of CD.
Programme
Project Grant
Bénéficiaire
Emplacement
Ontario, Canada
Type de bénéficiaire
Academia
Type
Grant
Source
CIHR Funding Decisions Database
Tel que publié
Id
488109
Name
Philpott Dana J
Region
Ontario
Country
Canada
Orgtype
Institution Paid; Research Institution
Instname2
Infection and Immunity
Theme2
Biomedical
Prcname2
Immunology
Projecttitle
Investigating the role of NOD2 in intestinal fibrosis
Programtype2
Operating Grants
Orgnameinp2
University of Toronto
Cihramount2
$994,500
Cihrequipment2
$0
Programname2
Project Grant
Keyworddelim
Crohn'S Disease; Fibrosis; Intestinal Inflammation; Nod2
Abstract
Intestinal fibrosis is a common debilitating complication associated with the inflammatorybowel disease (IBD), Crohn's disease (CD). There are no clinical solutions for preventing or treating fibrosis, except for surgical intervention. Therefore, there is a great unmet need to understand the mechanisms leading to fibrotic complications in CD. In general, fibrosis is a consequence of dysregulated healing processes. We have developed a mouse model of chronic intestinal inflammation where mice possess one of the gene variants associated with human CD develop fibrosis. Using this model, we can now determine how the process by which cells in the intestine promote fibrosis, which may reveal targetable pathways for the treatment or prevention of this severe complication of CD.
Competitiondate
202309
Approvedterm2
5 yrs 0 mth
Pinamesdelim
Philpott, Dana J
Approvedterm
5 ans 0 mois
Cihrcontribution2
~ $994,500~ $0~