On Day 3 (Thursday, October 29) of the American Society of Human Genetics (ASHG) 2020 Virtual Annual Meeting (https://www.ashg.org/meetings/2020meeting/), one of the multiple stimulating morning sessions was “From Genes to Therapeutic Targets and Clinical Trials” (#031) (https://www.abstractsonline.com/pp8/#!/9070/presentation/1474). Among the six presentations given during this session was a particularly interesting one titled “Genetic and Pharmacological Inhibition of Cholesteryl Ester Transfer Protein Improves Survival in Sepsis,” delivered by Mark Trinder (photo), MD/PhD Candidate and Vanier Scholar at the University of British Columbia, University of British Columbia. In the abstract to his talk, Trinder noted that sepsis is a dysregulated host response to infection that is responsible for up to 1 of 5 deaths globally. He said that numerous clinical trials have failed to identify drugs that improve outcomes from sepsis, suggesting the need for therapies that target pathways causal to the pathogenesis of the condition. Along these lines, he noted that high-density lipoprotein (HDL) particles, although best-known for their inverse association with coronary artery disease, possess many properties that are relevant to sepsis. The quantity of HDL, as reflected by the concentration of HDL cholesterol (HDL-C), declines drastically during severe infections such as sepsis and greater decline of HDL-C is associated with worse clinical outcomes. In the work described at the ASHG meeting, Trinder and colleagues tested the hypothesis that genetic or pharmacologic inhibition of cholesteryl ester transfer protein (CETP), which facilitates the metabolism of HDL-C, would decrease mortality from sepsis in humans and mice.
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