PMC:7373848 / 9665-10827 JSONTXT

{"target":"https://pubannotation.org/docs/sourcedb/PMC/sourceid/7373848","sourcedb":"PMC","sourceid":"7373848","source_url":"https://www.ncbi.nlm.nih.gov/pmc/7373848","text":"Endothelial glycocalyx degradation occurs in chronic disease states like diabetes mellitus [13], significantly impacting responses to acute infectious and metabolic conditions [14, 15] (Fig. 4).\nFig. 4 Structure of the endothelial glycocalyx/endothelial surface layer. a Endothelial glycocalyx thickness is larger than the endothelial cell itself, as demonstrated by electron microscopy of ruthenium-red labeled rat myocardial capillaries. In vivo, the glycocalyx forms an even more substantial ESL, with thickness \u003e 1 µm. b Pathological degradation of the glycocalyx/ESL during critical illnesses (such as sepsis) causes not only local endothelial injury, but also releases biologically active heparan sulfate fragments into the circulation that may influence signaling processes in an endocrine fashion. For simplicity, chondroitin sulfate and hyaluronic acid are not shown. α4 and β4 refer to glycosidic bonds connecting constituent saccharides. Inset: structure of a heparan sulfate octasaccharide fragment, demonstrating potential sites of sulfation within constituent disaccharide units\n(From Oshima K. Pulmonary Circulation 2017; 8: 1–10. 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