内皮糖萼在脓毒血症中的研究进展
Research Progress of Endothelial Glycocalyx in Sepsis
DOI: 10.12677/ACM.2023.13102361, PDF,   
作者: 何 锋*:承德医学院研究生学院,河北 承德;刘秀娟*#:秦皇岛市第一医院重症医学科一病区,河北 秦皇岛
关键词: 糖萼脓毒血症内皮损伤Glycocalyx Sepsis Endothelial Injury
摘要: 脓毒血症指局部器官或组织感染后细菌、毒素入血造成的多器官功能障碍,是一种由感染引起的全身炎症反应综合征(systemic inflammatory response syndrome, SIRS),其病死率高达30%~50%。糖萼作为血管内皮的组成,是覆盖于血管内皮细胞管腔侧表面的多绒毛状结构,它是炎症反应时最早被损伤的部位之一。研究内皮糖萼是诊治脓毒血症不可或缺的物质。这篇综述是对脓毒血症中糖萼研究进展的总结。
Abstract: Sepsis refers to the multiple organ dysfunction caused by the blood inflow of bacteria and toxins af-ter local organ or tissue infection. It is a systemic inflammatory response syndrome (SIRS) caused by infection, and its mortality rate is as high as 30%~50%. Calyx, as a component of vascular endo-thelium, is a multivilli structure covering the lumen surface of vascular endothelial cells. It is one of the earliest damaged parts during inflammation. Study on endothelial glycocalyx is an indispensa-ble substance in the diagnosis and treatment of sepsis. This review summarizes the research pro-gress of glycocalyx in sepsis.
文章引用:何锋, 刘秀娟. 内皮糖萼在脓毒血症中的研究进展[J]. 临床医学进展, 2023, 13(10): 16856-16862. https://doi.org/10.12677/ACM.2023.13102361

参考文献

[1] Rello, J., Valenzuela-Sánchez, F., Ruiz-Rodriguez, M., et al. (2017) Sepsis: A Review of Advances in Management. Advances in Therapy, 34, 2393-2411. [Google Scholar] [CrossRef] [PubMed]
[2] Robinson, B.D., Shaji, C.A., Lomas, A., et al. (2018) Measurement of Microvascular Endothelial Barrier Dysfunction and Hyperpermeability in Vitro. In: Tharakan, B., Ed., Traumatic and Ischemic Injury Methods and Protocols, Methods in Molecular Biology, Vol. 1717, Springer, Berlin, 237-242. [Google Scholar] [CrossRef] [PubMed]
[3] 翟建华, 卢斌, 刘晨燕, 等. 脓毒症患者毛细血管渗漏综合征的危险因素分析[J]. 继续医学教育, 2019, 33(5): 85-87.
[4] Chaudhry, H., Zhou, J., Zhong, Y., et al. (2013) Role of Cytokines as a Double-Edged Sword in Sepsis. In Vivo, 27, 669-684.
[5] Kumar, A. (2016) Systematic Bias in Meta-Analyses of Time to Antimicrobial in Sepsis Studies. Critical Care Medicine, 44, e234-e235. [Google Scholar] [CrossRef
[6] Miranda, M., Balarini, M., Caixeta, D., et al. (2016) Microcirculatory Dysfunction in Sepsis: Pathophysiology, Clinical Monitoring, and Potential Therapies. The American Journal of Physiology-Heart and Circulatory Physiology, 311, H24- H35. [Google Scholar] [CrossRef] [PubMed]
[7] Moore, K.H., Murphy, H.A. and George, E.M. (2021) The Gly-cocalyx: A Central Regulator of Vascular Function. American Journal of Physiology. Regulatory, Integrative and Com-parative Physiology, 320, R508-R518. [Google Scholar] [CrossRef] [PubMed]
[8] Purcell, S.C. and Godula, K. (2019) Synthetic Glycoscapes: Ad-dressing the Structural and Functional Complexity of the Glycocalyx. Interface Focus, 9, Article ID: 20180080. [Google Scholar] [CrossRef] [PubMed]
[9] Koo, A., Dewey, C.F. and García-Cardeña, G. (2013) Hemodynamic Shear Stress Characteristic of Atherosclerosis-Re- sistant Regions Promotes Glycocalyx Formation in Cultured Endothe-lial Cells. American Journal of Physiology-Cell Physiology, 304, C137-C146. [Google Scholar] [CrossRef] [PubMed]
[10] Iba, T. and Levy, J.H. (2019) Derangement of the Endothelial Glycocalyx in Sepsis. Journal of Thrombosis and Haemostasis, 17, 283-294. [Google Scholar] [CrossRef] [PubMed]
[11] Sperandio, M. (2006) Selectins and Glycosyltransferases in Leukocyte Roll-ing in Vivo. FEBS Journal, 273, 4377-4389. [Google Scholar] [CrossRef] [PubMed]
[12] Bombeli, T., Schwartz, B.R. and Harlan, J.M. (1998) Ad-hesion of Activated Platelets to Endothelial Cells: Evidence for a GPIIbIIIa-Dependent Bridging Mechanism and Novel Roles for Endothelial Intercellular Adhesion Molecule 1 (ICAM-1), αvβ3 Integrin, and GPIbalpha. Journal of Experi-mental Medicine, 187, 329-339. [Google Scholar] [CrossRef] [PubMed]
[13] Liu, H.Q., Li, J., Xuan, C.L. and Ma, H.C. (2020) A Review on the Physiological and Pathophysiological Role of Endothelial Glycocalyx. Journal of Biochemical and Molecular Toxicology, 34, e22571. [Google Scholar] [CrossRef] [PubMed]
[14] Pries, A.R., Secomb, T.W. and Gaehtgens, P. (2000) The En-dothelial Surface Layer. Pflügers Archiv, 440, 653-666. [Google Scholar] [CrossRef] [PubMed]
[15] Rapraeger, A., Jalkanen, M., Endo, E., et al. (1985) The Cell Surface Proteoglycan from Mouse Mammary Epithelial Cells Bears Chondroitin Sulfate and Heparan Sulfate Glycosaminogly-cans. Journal of Biological Chemistry, 260, 11046-11052.
[16] van den Berg, B.M., Nieuwdorp, M., Stroes, E.S., et al. (2006) Glycocalyx and Endothelial (dys) Function: From Mice to Men. Pharmacological Reports, 58, 75-80.
[17] Reitsma, S., Slaaf, D.W., Vink, H., et al. (2007) The Endothelial Glycocalyx: Composition, Functions, and Visualization. Pflügers Archiv, 454, 345-359. [Google Scholar] [CrossRef] [PubMed]
[18] Tarbell, J.M. (2010) Shear Stress and the Endothelial Transport Barrier. Cardiovascular Research, 87, 320-330. [Google Scholar] [CrossRef] [PubMed]
[19] Burke-Gaffney, A. and Evans, T.W. (2012) Lest We Forget the Endothelial Glycocalyx in Sepsis. Critical Care, 16, Article No. 121. [Google Scholar] [CrossRef] [PubMed]
[20] Chelazzi, C., Villa, G., Mancinelli, P., et al. (2015) Glycocalyx and Sepsis-Induced Alterations in Vascular Permeability. Critical Care, 19, Article No. 26. [Google Scholar] [CrossRef] [PubMed]
[21] Karamysheva, A.F. (2008) Mechanisms of Angi-ogenesis. Biochemistry (Moscow), 73, 751-762. [Google Scholar] [CrossRef
[22] Menger, M.D. and Vollmar, B. (2007) Pathomechanisms of Is-chemia-Reperfusion Injury as the Basis for Novel Preventive Strategies: Is It Time for the Introduction of Pleiotropic Compounds? Transplantation Proceedings, 39, 485- 488. [Google Scholar] [CrossRef] [PubMed]
[23] Alphonsus, C.S. and Rodseth, R.N. (2014) The Endotheli-al Glycocalyx: A Review of the Vascular Barrier. Anaesthesia, 69, 777-784. [Google Scholar] [CrossRef] [PubMed]
[24] Ziaja, M. (2013) Septic Encephalopathy. Current Neurology and Neuro-science Reports, 13, Article No. 383. [Google Scholar] [CrossRef] [PubMed]
[25] Margraf, A., Herter, J.M., Kühne, K., et al. (2018) 6% Hydroxy-ethyl Starch (HES 130/0.4) Diminishes Glycocalyx Degradation and Decreases Vascular Permeability during Systemic and Pulmonary Inflammation in Mice. Critical Care, 22, Article No. 111. [Google Scholar] [CrossRef] [PubMed]
[26] Zhu, J., Li, X., Yin, J., et al. (2018) Glycocalyx Degradation Leads to Blood-Brain Barrier Dysfunction and Brain Edema after Asphyxia Cardiac Arrest in Rats. Journal of Cerebral Blood Flow & Metabolism, 38, 1979-1992.
[27] Danielski, L.G., Giustina, A.D., Badawy, M., et al. (2018) Brain Bar-rier Breakdown as a Cause and Consequence of Neuroinflammation in Sepsis. Molecular Neurobiology, 55, 1045-1053. [Google Scholar] [CrossRef] [PubMed]
[28] Hempel, C., Sporring, J. and Kurtzhals, J.A.L. (2019) Experi-mental Cerebral Malaria Is Associated with Profound Loss of both Glycan and Protein Components of the Endothelial Glycocalyx. FASEB Journal, 33, 2058-2071. [Google Scholar] [CrossRef
[29] Hippensteel, J.A., Anderson, B.J., Orfila, J.E., et al. (2019) Circulating Heparan Sulfate Fragments Mediate Septic Cognitive Dysfunction. Journal of Clinical Investigation, 129, 1779-1784.
[30] Yang, Y. and Schmidt, E.P. (2013) The Endothelial Glycocalyx: An Important Regulator of the Pul-monary Vascular Barrier. Tissue Barriers, 1, e23494.
[31] Oshima, K., King, S.I., McMurtry, S.A., et al. (2021) Endo-thelial Heparan Sulfate Proteoglycans in Sepsis: The Role of the Glycocalyx. Seminars in Thrombosis and Hemostasis, 47, 274-282. [Google Scholar] [CrossRef] [PubMed]
[32] Chen, S., He, Y., Hu, Z., et al. (2017) Heparanase Me-diates Intestinal Inflammation and Injury in a Mouse Mode l of Sepsis. Journal of Histochemistry & Cytochemistry, 65, 241-249. [Google Scholar] [CrossRef] [PubMed]
[33] 颜娟, 曾志伟, 谢晓云. 肠上皮Syndecan-1对艰难梭菌所致腹泻患者的肠黏膜屏障保护作用分析[J]. 中国实用医药, 2018, 13(5): 35-36. [Google Scholar] [CrossRef
[34] White, L.E., Hassoun, H.T. and Bihorac, A. (2013) Acute Kidney Injury Is Surprisingly Common and a Powerful Predictor of Mortality in Surgical Sepsis. Journal of Trauma and Acute Care Surgery, 75, 432-438. [Google Scholar] [CrossRef
[35] Szymczak, M., Kuźniar, J. and Klinger, M. (2010) The Role of Heparanase in Diseases of the Glomeruli. Archivum Immunologiae et Therapiae Experimentalis (Warsz), 58, 45-56. [Google Scholar] [CrossRef] [PubMed]
[36] Meziani, F., Gando, S. and Vincent, J.L. (2017) Should All Pa-tients with Sepsis Receive Anticoagulation? Yes. Intensive Care Medicine, 43, 452-454. [Google Scholar] [CrossRef] [PubMed]
[37] Kozar, R.A. and Pati, S. (2015) Syndecan-1 Restitution by Plasma after Hemorrhagic Shock. Journal of Trauma and Acute Care Surgery, 78, S83-S86. [Google Scholar] [CrossRef
[38] DeAgostini, A.I., Watkins, S.C., Slayter, H.S., et al. (1990) Localization of Anticoagulantly Active Heparan Sulfate Proteoglycans in Vascular Endothelium: Antithrombin Binding on Cultured Endothelial Cells and Perfused Rat Aorta. Journal of Cell Biology, 111, 1293-1304. [Google Scholar] [CrossRef] [PubMed]
[39] Guo, C., Fan, X., Qiu, H., et al. (2015) High-Resolution Probing Hep-aran Sulfate-Antithrombin Interaction on a Single Endothelial Cell Surface: Single-Molecule AFM Studies. Physical Chemistry Chemical Physics, 17, 13301-13306. [Google Scholar] [CrossRef
[40] Bohdan, N., Espín, S., Águila, S., et al. (2016) Heparanase Activates Antithrombin through the Binding to Its Heparin Binding Site. PLOS ONE, 11, e0157834. [Google Scholar] [CrossRef] [PubMed]
[41] Marcum, J.A., McKenney, J.B. and Rosenberg, R.D. (1984) Acceleration of Thrombin-Antithrombin Complex Formation in Rat Hindquarters via Heparin-Like Molecules Bound to the Endothelium. Journal of Clinical Investigation, 74, 341-350. [Google Scholar] [CrossRef
[42] Margraf, A., Ludwig, N., Zarbock, A. and Rossaint, J. (2020) Systemic Inflammatory Response Syndrome after Surgery: Mecha-nisms and Protection. Anesthesia & Analgesia, 131, 1693-1707. [Google Scholar] [CrossRef