Forskningsbidrag fra Hjertefondet til:

A novel genetic integrin alpha11 mouse model: closing in on cardiac fibrosis

Om prosjektet:

It is estimated that fibrotic disorders contribute to 45% of all-cause mortality in the modern world. Cardiovascular diseases in turn cause approximately 31% of all deaths worldwide and cardicac fibrosis often contribute to heart failure. In cardiac fibrosis, we observe a pathological remodeling with increased stiffness, characterized by excessive depostion of collagen, and abnormal cardiac function.

When considering new therapies combating fibrosis, the importance of understanding the molecular mechanisms occuring in fibrotic niche, is increasingly beeing recognized. This interest extends to developing novel anti-stromal therapies targeting the fibrotic niche. Limited knowledge about gender differences as to biomarker expression and function also exists, although clinical data suggest that age related cardiac fibrosis is more prevalent in males.

Integrin a11 subunit (human gene name ITGA11), and the dimer a11b1 is a receptor for fibrillar collagens and is involved in tumor and tissue fibrosis. Our work into understanding integin a11b1 in the heart has involved several important collaborations. In 2018, we published a preliminary study on the role of a11 in heart fibrosis. Thansk to many years of basic research  on integrin a11, we now have unique animal models, cell lines, monoclonal antibodies and additional reagents to forcefully address basic research questions aimed at further understanding the role of a major collagen receptor on activated fibroblasts in cardiac fibrosis and exploring how to best employ this knowlegde in anti-fibrosis strategies. In addition to provididng mechanistic insight to an interesting fibroblast target we will also address the potential sex differences related to a11 in cardiac fibrosis.

Prosjektstøtte fra Hjertefondet tildeles forsker Cedric Zeltz.



Kr. 100.000