Robert Hebbel

Robert Hebbel, MD

RobeRobert Hebbelrt P. Hebbel received the MD degree from University of Minnesota in1973, thereafter training in Internal Medicine (University of Washington) and Hematology (University of Minnesota).

He joined the faculty of the Department of Medicine at the University of Minnesota Medical school in 1979, where he is currently Regents Professor and Clark Professor, and Director of the Vascular Biology Center.

His laboratory has focused upon the vascular pathobiology of sickle disease since 1977 and, with a shift of focus to the vascular endothelium 15+ years ago, he embraced a systems biology perspective on sickle disease. Current studies address the fundamental concept that endothelial dysfunction comprises the central linkage between the sickle mutation and clinical disease.

Hebbel also has an active program in other areas of vascular biology, most notably related to endothelial progenitor cells. He continues active programs in the use of their progeny (blood outgrowth endothelial cells) for gene therapy of cancer and pulmonary hypertension, as well as for studies that identify genetically determined inter-individual differences in endothelial cell biology that may underlie heterogeneities of clinical phenotype (eg, sickle with vs without Circle of Willis disease).

The latter has led to a convergence of his long-standing interests in the pathobiology of sickle stroke on the one hand and minority cardiovascular health disparity on the other. This is the other main focus of his laboratory’s programs.


The hyper-hemolysis paradigm from the perspectives of systems biology

The hyper-hemolysis paradigm for explaining the pathogenesis of pulmonary hypertension in sickle disease is intriguing and seemingly logical, and it has been widely accepted. However, careful consideration of the actual evidence underpinning the paradigm’s component steps identifies a number of weaknesses that jeopardize the paradigm’s validity. Therefore, the veracity of its key evidentiary observations will be discussed, using the classical criteria of Sir Bradford Hill (for validity of clinical research) as a guideline. That the disparate vasculopathic complications of this disease even have a common, single, underlying pathophysiology is the most parsimonious view, but this may or may not be true. Indeed, a rationale for believing different processes dominate vasculopathy in different vascular beds will be considered. In addition, a plausible systems biological structure for understanding the pathophysiology of sickle vasculopathy will be presented.

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