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糖萼与动脉粥样硬化的研究进展
作者:
作者单位:

(海军军医大学附属长海医院心内科,上海市200433)

作者简介:

努尔柯孜·阿卜杜合力力,硕士研究生,研究方向为冠状动脉粥样硬化性心脏病,E-mail:3445775378@qq.com。

基金项目:

国家自然科学基金(81760076,82070419)


Progress in the glycocalyx and atherosclerosis
Author:
Affiliation:

Department of Cardiology, Changhai Hospital, Naval Military Medical University, Shanghai 200433, China)

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    摘要:

    动脉粥样硬化(As)是心脑血管疾病中最常见的病变,血管内皮功能障碍是As的初始阶段,糖萼(GCX)作为血管内皮表面覆盖的物理屏障,可通过调节血管通透性、舒张功能、细胞间通讯及炎症细胞黏附等,参与As的发生发展。因此,保持血管内皮GCX完整性可能是As治疗的潜在靶点。此外,GCX脱落水平可反映As严重程度。因此,GCX降解产物水平(如硫酸乙酰肝素、透明质酸等)可能用于评估As的严重程度。本文就GCX在As发生中的研究进展进行综述。

    Abstract:

    Atherosclerosis is the most common disease in cardiovascular and cerebrovascular diseases, and vascular endothelial dysfunction is the initial stage of atherosclerosis. As a physical barrier between the flowing blood and the endothelium,glycocalyx can participate in the occurrence and development of atherosclerosis by regulating vascular permeability, diastolic function, intercellular communication and inflammatory cell adhesion. Therefore, the maintenance or restoration of the integrity of the glycocalyx may be a potential therapeutic target for atherosclerosis. Moreover, the abscission level of glycocalyx can reflect the severity of atherosclerosis. Therefore, the level of glycocalyx degradation products (such as acetheparan sulfate, hyaluronic acid, etc) may be used to evaluate the severity of atherosclerosis in the future. This review summarizes the research progress of glycocalyx in atherogenesis.

    参考文献
    [1] LUK C, HAYWOOD N J, BRIDGE K I, et al.Paracrine role of the endothelium in metabolic homeostasis in health and nutrient excess.Front Cardiovasc Med, 2,9:882923.
    [2] GEOVANINI G R, LIBBY P.Atherosclerosis and inflammation:overview and updates.Clin Sci (Lond), 8,2(12):1243-1252.
    [3] XUE X J, JIANG Y, CHEN L, et al.Relationship between the endothelial glycocalyx and the extent of coronary atherosclerosis.Microcirculation, 8,5(8):e12504.
    [4] CANCEL LM, EBONG EE, MENSAH S, et al.Endothelial glycocalyx, apoptosis and inflammation in an atherosclerotic mouse model.Atherosclerosis, 6,2:136-146.
    [5] PILLINGER N L, KAM P.Endothelial glycocalyx:basic science and clinical implications.Anaesth Intensive Care, 7,5(3):295-307.
    [6] FOOTE C A, SOARES R N, RAMIREZ-PEREZ F I, et al.Endothelial glycocalyx.Compr Physiol, 2,2(4):3781-3811.
    [7] JEDLICKA J, BECKER B F, CHAPPELL D.Endothelial glycocalyx.Crit Care Clin, 0,6(2):217-232.
    [8] ABASSI Z, ARMALY Z, HEYMAN S N.Glycocalyx degradation in ischemia-reperfusion injury.Am J Pathol, 0,0(4):752-767.
    [9] FISCHER J W.Role of hyaluronan in atherosclerosis:current knowledge and open questions.Matrix Biol, 9,8/79:324-336.
    [10] CHENG M J, KUMAR R, SRIDHAR S, et al.Endothelial glycocalyx conditions influence nanoparticle uptake for passive targeting.Int J Nanomedicine, 6,1:3305-3315.
    [11] KANG H Y, YANG J L, ZHANG W C, et al.Effect of endothelial glycocalyx on water and LDL transport through the rat abdominal aorta.Am J Physiol Heart Circ Physiol, 1,0(4):H1724-H1737.
    [12] MITRA R, O'NEIL GL, HARDING IC.Glycocalyx in atherosclerosis-relevant endothelium function and as a therapeutic target.Curr Atheroscler Rep, 7,9(12):63.
    [13] WANG L P, HUANG X, KONG G Q, et al.Ulinastatin attenuates pulmonary endothelial glycocalyx damage and inhibits endothelial heparanase activity in LPS-induced ARDS.Biochem Biophys Res Commun, 6,8(2):669-675.
    [14] YING J, ZHANG C, WANG Y, et al.Sulodexide improves vascular permeability via glycocalyx remodelling in endothelial cells during sepsis.Front Immunol, 3,4:1172892.
    [15] CHENG M J, BAL N N, PRABAKARAN P, et al.Ultrasmall gold nanorods:synthesis and glycocalyx-related permeability in human endothelial cells.Int J Nanomedicine, 9,4:319-333.
    [16] RAMADAN R, BAATOUT S, AERTS A, et al.The role of connexin proteins and their channels in radiation-induced atherosclerosis.Cell Mol Life Sci, 1,8(7):3087-3103.
    [17] 李建军, 林宏, 李柱一, 等.辛伐他丁减少Connexin43表达和兔粥样硬化斑块形成.第四军医大学学报, 5,6(21):2006-2009.LI J J, LIN H, LI Z Y, et al.Simvastatin reduces Connexin43 expression and inhibits rabbit atherosclerotic lesion formation.J Air Force Med Univ, 5,6(21):2006-2009.
    [18] MENSAH S A, CHENG M J, HOMAYONI H, et al.Regeneration of glycocalyx by heparan sulfate and sphingosine 1-phosphate restores inter-endothelial communication.PLoS One, 7,2(10):e0186116.
    [19] MENSAH S A, NERSESYAN A A, EBONG E E.Endothelial glycocalyx-mediated intercellular interactions:mechanisms and implications for atherosclerosis and cancer metastasis.Cardiovasc Eng Technol, 1,2(1):72-90.
    [20] TAMARGO I A, BAEK K I, KIM Y, et al.Flow-induced reprogramming of endothelial cells in atherosclerosis.Nat Rev Cardiol, 3,0(11):738-753.
    [21] ZHOU M, YU Y, CHEN R, et al.Wall shear stress and its role in atherosclerosis.Front Cardiovasc Med, 3,0:1083547.
    [22] KANG H Y, SUN Q N, WU Q H, et al.Atherogenic diet-diminished endothelial glycocalyx contributes to impaired vasomotor properties in rat.Am J Physiol Heart Circ Physiol, 0,9(4):H814-H823.
    [23] CHO J M, LY K, LY S, et al.Procedures to evaluate the role of heparan sulfate on the reactivity of resistance and conductance arteries ex vivo.Methods Mol Biol, 2,3:495-511.
    [24] DABAGH M, JALALI P, BUTLER P J, et al.Mechanotransmission in endothelial cells subjected to oscillatory and multi-directional shear flow.J R Soc Interface, 7,4(130):20170185.
    [25] HARDING I C, MITRA R, MENSAH S A, et al.Pro-atherosclerotic disturbed flow disrupts caveolin-1 expression, localization, and function via glycocalyx degradation.J Transl Med, 8,6(1):364.
    [26] WEINBAUM S, CANCEL L M, FU B M, et al.The glycocalyx and its role in vascular physiology and vascular related diseases.Cardiovasc Eng Technol, 1,2(1):37-71.
    [27] BARTOSCH A M W, MATHEWS R, MAHMOUD M M, et al.Heparan sulfate proteoglycan glypican-1 and PECAM-1 cooperate in shear-induced endothelial nitric oxide production.Sci Rep, 1,1(1):11386.
    [28] MAHMOUD M, MAYER M, CANCEL L M, et al.The glycocalyx core protein Glypican 1 protects vessel wall endothelial cells from stiffness-mediated dysfunction and disease.Cardiovasc Res, 1,7(6):1592-1605.
    [29] WAUTIER J L, WAUTIER M P.Vascular permeability in diseases.Int J Mol Sci, 2,3(7):3645.
    [30] MENSAH S A, NERSESYAN A A, HARDING I C, et al.Flow-regulated endothelial glycocalyx determines metastatic cancer cell activity.FASEB J, 0,4(5):6166-6184.
    [31] MENSAH S A, HARDING I C, ZHANG M, et al.Metastatic cancer cell attachment to endothelium is promoted by endothelial glycocalyx sialic acid degradation.AIChE J, 9,5(8):e16634.
    [32] DELGADILLO L F, LOMAKINA E B, KUEBEL J, et al.Changes in endothelial glycocalyx layer protective ability after inflammatory stimulus.Am J Physiol Cell Physiol, 1,0(2):C216-C224.
    [33] SIEVE I, MNSTER-KHNEL AK, HILFIKER-KLEINER D.Regulation and function of endothelial glycocalyx layer in vascular diseases.Vascul Pharmacol, 8,0:26-33.
    [34] ZHANG J J, KONG X Q, WANG Z M, et al.AMP-activated protein kinase regulates glycocalyx impairment and macrophage recruitment in response to low shear stress.FASEB J, 9,3(6):7202-7212.
    [35] CROMPTON M, SKINNER L J, SATCHELL S C, et al.Aldosterone:essential for life but damaging to the vascular endothelium.Biomolecules, 3,3(6):1004.
    [36] JIANG X Z, GOLIGORSKY M S.Biomechanical properties of endothelial glycocalyx:an imperfect pendulum.Matrix Biol Plus, 1,2:100087.
    [37] HARA T, KONISHI T, YASUIKE S, et al.Sb-phenyl-N-methyl-5,6,7,2-tetrahydrodibenz [c,f][1,5] azastibocine induces perlecan core protein synthesis in cultured vascular endothelial cells.Int J Mol Sci, 3,4(4):3656.
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努尔柯孜·阿卜杜合力力,吴弘.糖萼与动脉粥样硬化的研究进展[J].中国动脉硬化杂志,2024,32(11):994~998.

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  • 收稿日期:2023-12-07
  • 最后修改日期:2024-01-03
  • 在线发布日期: 2024-11-22

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