James Faber, PhD
Education and Training
University of Missouri-Columbia, BS, 1974
University of Missouri-Columbia, PhD, 1980
University of Iowa Cardiovascular Center, Postdoctoral, 1983
Areas of Interest
My lab focuses on the vascular biology of the collateral circulation. We have found that the abundance of collaterals—unique “endogenous bypass vessels” that are present in the microcirculation of most tissues—vary >50-fold among inbred and wild-derived mice due to naturally occurring differences in genetic background. This wide variation is finding confirmation in humans. A consequence is that individuals with poor collateral abundance suffer greater tissue injury when arterial obstruction occurs. The result is much more severe stroke, myocardial infarction, ischemic heart disease, and peripheral artery disease. Current work is focused on identifying the genes and their signaling pathways responsible for this variation. We have found that naturally occurring variants of a single novel gene account for most of the variation in mouse through this gene’s primary role in governing the formation of collaterals—which occurs in the embryo. Identification of the collaterogenesis pathway that this gene drives has led to the discovery that new collaterals can be induced to form in adult tissues. A prospective study involving 11 stroke centers began in 2015 to determine if the same or related gene(s) is responsible for collateral insufficiency in humans. We have also identified a retinal biomarker for collateral abundance in mouse which will soon begin testing in humans. These findings could provide novel diagnostic markers and therapeutic targets for stroke, heart disease, and peripheral artery disease. We have found that hypertension, diabetes and hyperlipidemia, as well as advanced age and Alzheimer’s disease cause selective loss of collateral vessels. Ongoing studies are addressing the responsible mechanisms, with the goal of identifying preventive therapies.