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Three decades ago a revolutionary idea was born that ascribed to dysfunctional endothelia some manifestations of diabetes, the Steno hypothesis, so named after the Steno Diabetes Center, Gentofte, in Denmark. Here I briefly outline the accomplishments accrued in the past 15 years to buttress this hypothesis. Those include development of novel technological platforms to examine microcirculatory beds, deeper understanding of patterns of microvascular derangement in diabetes, pathophysiology of nitric oxide synthesis and availability, nitrosative and oxidative stress in diabetes, premature senescence of endothelial cells and the role of sirtuin 1 and lysosomal dysfunction in this process, and the state of endothelial glycocalyx and endothelial progenitor cells in diabetes. These pathophysiological findings may yield some therapeutic benefits.
Michael S. Goligorsky (Thu,) studied this question.