Inhibition of Cholesteryl Ester Transfer Protein Preserves High-Density Lipoprotein Cholesterol and Improves Survival in Sepsis
This week we profile a recent publication in Circulation from Mark Trinder (pictured)
in the laboratory of Dr. Liam Brunham at the Centre for Heart Lung Innovation.
Can you provide a brief overview of your lab’s current research focus?
Our research focuses on genetic regulation of lipid levels, and in particular the role of lipid metabolism in sepsis and severe infections.
What is the significance of the findings in this publication?
Our previous research identified that people with a gain-of-function DNA variant in a gene called CETP have lower levels of HDL cholesterol (the “good cholesterol”) during sepsis and a higher risk of death. In this study, we tested the hypothesis that inhibiting CETP using a drug would improve outcomes from sepsis. We performed this work in a mouse model of experimental sepsis, and showed that inhibiting CETP resulted in preservation of HDL levels and improved survival from sepsis.
What are the next steps for this research?
Our next steps are to design a clinical trial to study the usefulness of this medication in patients with sepsis, as well as to more fully understand the mechanisms by which HDL improves outcomes from sepsis.
This work was funded by:
This study is supported by a project grant from CIHR. We also had a pilot grant from the Providence Health Care Research Institute.