Geert W. Schmid-Schönbein is Distinguished Professor in the Department of Bioengineering at the University of California San Diego (UCSD). He teaches bioengineering and biomechanics of living tissues, microcirculation, lymphology, and biorheology, cell and molecular biomechanics with application to human diseases. Schmid-Schönbein was President of the Microcirculatory SocietyPresident of the Biomedical Engineering Society and serves as a consultant for the National Institute of Health, is a Founding Member of the American Institute for Medical and Biological Engineering, and was Chair of the World Council for Biomechanics.
The current research focus of his team is to answer a fundamental question: What are the trigger mechanisms for inflammation that cause diverse tissue injuries and organ dysfunctions? His team discovered a mechanism due to pancreatic digestive enzymes, which they designated “Autodigestion”. It is due to a leak of pancreatic digestive enzymes across the mucin/epithelial barrier out of the gastrointestinal tract into the circulation and peripheral organs. The team provided evidence that cell dysfunctions in Metabolic Syndrome X are due to unchecked activity by pancreatic digestive proteases leaking out of the gastrointestinal tract. The digestive enzymes activate secondary proteases and cause cleavage of the extracellular domain of membrane receptors, for example, in addition to many other cell dysfunctions, insulin resistance due to cleavage of the insulin receptor ectodomain or capillary rarefaction due to cleavage of endothelial growth factor receptors and endothelial apoptosis. Furthermore, the team showed in acute hemorrhagic and septic shock, pancreatic digestive enzymes leak in high concentrations out of the gastrointestinal tract and cause severe cell dysfunction, leading to complete organ failures. The team has shown that enteral blockade of pancreatic digestive enzymes attenuates acute organ dysfunctions in shock and reduces morbidity. Schmid-Schönbein proposes that Autodigestion may be a fundamental mechanism for aging, disease, and death.