The University of Washington has received a USD 1.2 million NHLBI R35 award to investigate how diabetes accelerates cardiovascular disease in youth, with principal investigator Karin Bornfeldt leading a seven-year translational program targeting triglyceride-rich lipoprotein biology as a driver of residual cardiovascular risk.
The grant, funded through the National Heart, Lung, and Blood Institute, centers on apolipoprotein C3 (APOC3) and its role in governing triglyceride-rich lipoprotein (TRL) and remnant lipoprotein particle (RLP) subpopulations. The central hypothesis is that adipose tissue insulin resistance in both type 1 and type 2 diabetes drives excess hepatic APOC3 production, causing accumulation of a mid-sized atherogenic TRL subpopulation that promotes vascular inflammation and early arterial stiffening. The program combines longitudinal studies in youth with diabetes with mechanistic work in mouse models and cell systems, and includes investigation of the hepatic sortilin 1–APOB100 secretion pathway as a potential mechanism underlying elevated APOC3 and accelerated atherosclerosis.
Funding context and translational relevance
The R35 mechanism, administered by NHLBI, is designed to provide sustained investigator support over extended project periods. The current award covers FY2026 costs of USD 1,233,682, with a project window running to February 2033. Bornfeldt, who holds an h-index of 63 across 448 publications, has been affiliated with the University of Washington since the mid-1990s and has published extensively on diabetes-associated atherosclerosis. The focus on youth-onset type 2 diabetes is notable given epidemiological projections suggesting a substantial rise in pediatric incidence over coming decades, a population in which LDL-lowering alone leaves a well-documented residual cardiovascular risk linked to dyslipidemia beyond LDL cholesterol. NHLBI's decision to fund a long-horizon mechanistic and clinical program in this area reflects continued interest in lipoprotein subfractionation and novel biomarker development as tools for cardiovascular risk stratification in metabolic disease.
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