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Novel aspects of fibrin(ogen) fragments during inflammation.在炎症过程中纤维蛋白(原)片段的新方面。
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2
Release of fibrinopeptides by the slow and fast forms of thrombin.凝血酶的慢速和快速形式释放纤维蛋白肽。
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Clottability and cross-linking reactivity of fibrin(ogen) following differential release of fibrinopeptides A and B.纤维蛋白肽A和B差异释放后纤维蛋白原的可凝性和交联反应性
Thromb Haemost. 1976 Dec 31;36(3):582-92.
4
Fibrinopeptides A and B release in the process of surface fibrin formation.纤维蛋白肽 A 和 B 在表面纤维蛋白形成过程中释放。
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A two-step fibrinogen--fibrin transition in blood coagulation.血液凝固过程中纤维蛋白原向纤维蛋白的两步转变。
Nature. 1978 Oct 12;275(5680):501-5. doi: 10.1038/275501a0.
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Conversion of fibrinogen to fibrin induced by preferential release of fibrinopeptide B.纤维蛋白肽B的优先释放诱导纤维蛋白原向纤维蛋白的转化。
Biochim Biophys Acta. 1989 Jan 27;990(1):18-24. doi: 10.1016/s0304-4165(89)80006-6.
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Fibrin polymerization sites in fibrinogen and fibrin fragments.纤维蛋白原和纤维蛋白片段中的纤维蛋白聚合位点。
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The sequence of cleavage of fibrinopeptides from fibrinogen is important for protofibril formation and enhancement of lateral aggregation in fibrin clots.从纤维蛋白原上裂解纤维蛋白肽的顺序对于原纤维形成和纤维蛋白凝块中侧向聚集的增强很重要。
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Structural basis for sequential cleavage of fibrinopeptides upon fibrin assembly.纤维蛋白组装时纤维蛋白肽顺序裂解的结构基础。
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High metabolic activity in positron emission tomography and systemic inflammation occurring years after exposure cessation in engineered stone silicosis.在工程石矽肺中,暴露停止数年之后,正电子发射断层扫描显示出高代谢活性以及全身性炎症。
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本文引用的文献

1
The fibrin-derived peptide Bbeta(15-42) significantly attenuates ischemia-reperfusion injury in a cardiac transplant model.纤维蛋白衍生肽 Bbeta(15-42)可显著减轻心脏移植模型中的缺血再灌注损伤。
Transplantation. 2010 Apr 15;89(7):824-9. doi: 10.1097/tp.0b013e3181ccd822.
2
Blood coagulation disorders in septic patients.脓毒症患者的凝血功能障碍
Wien Med Wochenschr. 2010 Mar;160(5-6):129-38. doi: 10.1007/s10354-009-0738-9.
3
Cellular sources of tissue factor in endotoxemia and sepsis.内毒素血症和脓毒症中的组织因子细胞来源。
Thromb Res. 2010 Apr;125 Suppl 1:S70-3. doi: 10.1016/j.thromres.2010.01.042. Epub 2010 Feb 24.
4
Enhancement of fibrinogen-triggered pro-coagulant activation of monocytes in vitro by matrix metalloproteinase-9.基质金属蛋白酶-9体外增强纤维蛋白原触发单核细胞的促凝活性。
Thromb J. 2010 Jan 29;8(1):2. doi: 10.1186/1477-9560-8-2.
5
The coagulant response in sepsis and inflammation.脓毒症和炎症中的凝血反应。
Hamostaseologie. 2010 Jan;30(1):10-2, 14-6.
6
Plasminogen on the surfaces of fibrin clots prevents adhesion of leukocytes and platelets.纤维蛋白凝块表面的纤溶酶原可防止白细胞和血小板黏附。
J Thromb Haemost. 2010 Apr;8(4):799-807. doi: 10.1111/j.1538-7836.2010.03778.x. Epub 2009 Jan 22.
7
A novel fragment derived from the beta chain of human fibrinogen, beta43-63, is a potent inhibitor of activated endothelial cells in vitro and in vivo.一种源自人纤维蛋白原β链的新型片段,β43-63,是体外和体内激活的内皮细胞的有效抑制剂。
Br J Cancer. 2010 Feb 2;102(3):594-601. doi: 10.1038/sj.bjc.6605495. Epub 2010 Jan 12.
8
Peptide Bbeta(15-42) preserves endothelial barrier function in shock.肽Bβ(15 - 42)在休克中可维持内皮屏障功能。
PLoS One. 2009;4(4):e5391. doi: 10.1371/journal.pone.0005391. Epub 2009 Apr 29.
9
Effect of intravenous FX06 as an adjunct to primary percutaneous coronary intervention for acute ST-segment elevation myocardial infarction results of the F.I.R.E. (Efficacy of FX06 in the Prevention of Myocardial Reperfusion Injury) trial.静脉注射FX06作为急性ST段抬高型心肌梗死直接经皮冠状动脉介入治疗辅助手段的效果:F.I.R.E.(FX06预防心肌再灌注损伤的疗效)试验结果
J Am Coll Cardiol. 2009 Feb 24;53(8):720-9. doi: 10.1016/j.jacc.2008.12.017.
10
Bbeta15-42 (FX06) reduces pulmonary, myocardial, liver, and small intestine damage in a pig model of hemorrhagic shock and reperfusion.β15-42(FX06)可减轻失血性休克和再灌注猪模型中的肺、心肌、肝脏及小肠损伤。
Crit Care Med. 2009 Feb;37(2):598-605. doi: 10.1097/CCM.0b013e3181959a12.

在炎症过程中纤维蛋白(原)片段的新方面。

Novel aspects of fibrin(ogen) fragments during inflammation.

机构信息

Clinic of Anesthesiology, Intensive Care Medicine and Pain Therapy, Goethe-University Hospital Frankfurt, Frankfurt am Main, Germany.

出版信息

Mol Med. 2011 May-Jun;17(5-6):568-73. doi: 10.2119/molmed.2010.00146. Epub 2011 Jan 4.

DOI:10.2119/molmed.2010.00146
PMID:21210072
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3105136/
Abstract

Coagulation is fundamental for the confinement of infection and/or the inflammatory response to a limited area. Under pathological inflammatory conditions such as arthritis, multiple sclerosis or sepsis, an uncontrolled activation of the coagulation system contributes to inflammation, microvascular failure and organ dysfunction. Coagulation is initiated by the activation of thrombin, which, in turn, triggers fibrin formation by the release of fibrinopeptides. Fibrin is cleaved by plasmin, resulting in clot lysis and an accompanied generation of fibrin fragments such as D and E fragments. Various coagulation factors, including fibrinogen and/or fibrin [fibrin(ogen)] and also fibrin degradation products, modulate the inflammatory response by affecting leukocyte migration and cytokine production. Fibrin fragments are mostly proinflammatory, however, Bβ15-42 in particular possesses potential antiinflammatory effects. Bβ15-42 inhibits Rho-kinase activation by dissociating Fyn from Rho and, hence prevents stress-induced loss of endothelial barrier function and also leukocyte migration. This article summarizes the state-of-the-art in inflammatory modulation by fibrin(ogen) and fibrin fragments. However, further research is required to gain better understanding of the entire role fibrin fragments play during inflammation and, possibly, disease development.

摘要

凝血对于感染的局限和/或炎症反应的局限是至关重要的。在关节炎、多发性硬化症或败血症等病理炎症条件下,凝血系统的失控激活会导致炎症、微血管衰竭和器官功能障碍。凝血是通过凝血酶的激活启动的,凝血酶反过来通过释放纤维蛋白肽触发纤维蛋白的形成。纤维蛋白被纤溶酶裂解,导致血栓溶解,并伴随纤维蛋白片段(如 D 和 E 片段)的产生。各种凝血因子,包括纤维蛋白原和/或纤维蛋白(原)以及纤维蛋白降解产物,通过影响白细胞迁移和细胞因子产生来调节炎症反应。纤维蛋白片段大多具有促炎作用,但 Bβ15-42 尤其具有潜在的抗炎作用。Bβ15-42 通过将 Fyn 从 Rho 上解离来抑制 Rho-激酶的激活,从而防止应激诱导的内皮屏障功能丧失和白细胞迁移。本文总结了纤维蛋白原和纤维蛋白片段对炎症的调节的最新进展。然而,需要进一步的研究来更好地理解纤维蛋白片段在炎症期间以及可能在疾病发展过程中所起的全部作用。