Dr Faber's recent work has found that the number and diameter of collaterals—unique "endogenous bypass vessels" that are present in brain, heart, lower extremities and other tissues—vary widely among healthy mice. This discovery is now finding confirmation in humans. A consequence is that individuals with poor collateral abundance suffer greater tissue injury and cell death when arterial occlusion occurs secondary to thrombosis, embolism or atherosclerosis. The result is much more severe stroke, myocardial infarction, ischemic heart disease, and peripheral artery disease. Current work by the Faber group is focused on determining the genetic and environmental factors responsible for this variation. They have identified a single genetic locus that is responsible for 75-85% of the variation in mice. Ongoing work is directed at identifying the underlying gene and the collaterogenesis pathway that it controls, and determining if a similar "risk allele" is responsible for collateral insufficiency in humans. Answers to these questions could provide novel diagnostic markers and therapeutic targets for stroke, heart disease, and peripheral artery disease.
Dr. Faber received his PhD degree in Physiology from the University of Missouri in 1980. He then joined the laboratory of Dr. Michael Brody at the University of Iowa as a Postdoctoral Fellow in Pharmacology. In 1983 Dr. Faber became Assistant Professor in the Department of Cell and Molecular Physiology at University of North Carolina and was appointed Professor in 1994.
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