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心内膜炎免疫血栓形成

Endocarditis Immunothrombosis.

作者信息

Nappi Francesco

机构信息

Department of Cardiac Surgery, Centre Cardiologique du Nord, 93200 Saint-Denis, France.

出版信息

Metabolites. 2025 May 15;15(5):328. doi: 10.3390/metabo15050328.


DOI:10.3390/metabo15050328
PMID:40422904
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12114098/
Abstract

Infective endocarditis continues to represent a challenge for healthcare systems, requiring careful management and resources. Recent studies have indicated a shift in the predominant pathogens of concern, with sp. a being superseded by sp. and sp. as the leading causes of concern. This shift is of concern as it is associated with which has a high virulence rate and a tendency to form a biofilm, meaning that non-surgical therapy may not be effective. It is imperative to deliberate on the likelihood of platelet blood clot formation, which may be accompanied by bacterial infestation and the development of a biofilm. MEDLINE, Embase, and Pubmed were searched using terms relating to 'endocarditis' and '', along with 'epidemiology', 'pathogenesis', 'coagulation', 'platelet', 'aggregation', and 'immunity'. The search focused on publications from the past 15 years, but excluded older, highly regarded articles. We also searched the reference lists of relevant articles. Recommended review articles are cited for more details. An endocarditis lesion is believed to be a blood clot infected with bacteria that adheres to the heart valves. Infective endocarditis is a good example of immunothrombosis, where the coagulation system, innate immunity and the function of coagulation in isolating and eliminating pathogens interact. However, in the context of infective endocarditis, immunothrombosis unintentionally establishes an environment conducive to bacterial proliferation. The process of immunothrombosis impedes the immune system, enabling bacterial proliferation. The coagulation system plays a pivotal role in the progression of this condition. The coagulation system is key to how bacteria attach to the heart valves, how vegetations develop, and how complications like embolisation and valve dysfunction occur. , the main cause of infective endocarditis, can change blood clotting, growing well in the fibrin-rich environment of vegetation. The coagulation system is a good target for treating infective endocarditis because of its central role in the disease. But we must be careful, as using blood-thinning medicines in patients with endocarditis can often lead to an increased risk of bleeding.

摘要

感染性心内膜炎仍然是医疗系统面临的一项挑战,需要精心管理和投入资源。最近的研究表明,主要关注的病原体发生了变化,A 种链球菌已被 B 种链球菌和 C 种链球菌取代,成为主要的关注病因。这种转变令人担忧,因为它与高毒力率以及形成生物膜的倾向有关,这意味着非手术治疗可能无效。必须考虑血小板血栓形成的可能性,这可能伴有细菌感染和生物膜的形成。使用与“心内膜炎”和“特定细菌名称”相关的术语,以及“流行病学”“发病机制”“凝血”“血小板”“聚集”和“免疫”等词,对 MEDLINE、Embase 和 Pubmed 进行了检索。检索重点是过去 15 年的出版物,但排除了较旧的、备受推崇的文章。我们还检索了相关文章的参考文献列表。推荐的综述文章有更详细的引用。心内膜炎病变被认为是附着在心脏瓣膜上的被细菌感染的血栓。感染性心内膜炎是免疫血栓形成的一个很好的例子,其中凝血系统、固有免疫以及凝血在隔离和消除病原体中的作用相互作用。然而,在感染性心内膜炎的背景下,免疫血栓形成无意中创造了一个有利于细菌增殖的环境。免疫血栓形成过程阻碍了免疫系统,使细菌得以增殖。凝血系统在这种疾病的进展中起着关键作用。凝血系统对于细菌如何附着在心脏瓣膜上、赘生物如何形成以及栓塞和瓣膜功能障碍等并发症如何发生至关重要。特定细菌名称作为感染性心内膜炎的主要病因,可改变血液凝固,在富含纤维蛋白的赘生物环境中生长良好。由于凝血系统在该疾病中起核心作用,因此它是治疗感染性心内膜炎的一个良好靶点。但我们必须小心,因为在心内膜炎患者中使用血液稀释药物通常会导致出血风险增加。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/a571e42a5a42/metabolites-15-00328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/65add43598dd/metabolites-15-00328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/4cc92c7343c6/metabolites-15-00328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/4fe75a85b070/metabolites-15-00328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/72ff53d59082/metabolites-15-00328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/a571e42a5a42/metabolites-15-00328-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/65add43598dd/metabolites-15-00328-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/4cc92c7343c6/metabolites-15-00328-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/4fe75a85b070/metabolites-15-00328-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/72ff53d59082/metabolites-15-00328-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a20f/12114098/a571e42a5a42/metabolites-15-00328-g005.jpg

相似文献

[1]
Endocarditis Immunothrombosis.

Metabolites. 2025-5-15

[2]
Coagulation: At the heart of infective endocarditis.

J Thromb Haemost. 2020-5

[3]
Neutrophils Protect Against Endocarditis Progression Independent of Extracellular Trap Release.

Arterioscler Thromb Vasc Biol. 2023-2

[4]
Host-Bacterium Interaction Mechanisms in Endocarditis: A Systematic Review.

Int J Mol Sci. 2023-7-4

[5]
Isolated Pulmonary Valve Infective Endocarditis With Persistent Staphylococcus aureus Bacteremia and Rapid Clearance With Ertapenem Plus Cefazolin.

Cureus. 2025-1-12

[6]
Type IV Pili of Streptococcus sanguinis Contribute to Pathogenesis in Experimental Infective Endocarditis.

Microbiol Spectr. 2021-12-22

[7]
Platelet receptor polymorphisms do not influence Staphylococcus aureus-platelet interactions or infective endocarditis.

Microbes Infect. 2010-10-29

[8]
Phenotypes and Virulence among Staphylococcus aureus USA100, USA200, USA300, USA400, and USA600 Clonal Lineages.

mSphere. 2016-6-8

[9]
Aspirin or Ticagrelor in Infective Endocarditis: Where Do We Stand?

Front Cell Dev Biol. 2021-10-7

[10]
Role of monocytes in experimental Staphylococcus aureus endocarditis.

Infect Immun. 2000-8

本文引用的文献

[1]
Extracellular adherence proteins reduce matrix porosity and enhance biofilm survival during prosthetic joint infection.

Infect Immun. 2025-4-8

[2]
Cooperation between coagulase and von willebrand factor binding protein in fibrin pseudocapsule formation.

Biofilm. 2024-10-23

[3]
Native Infective Endocarditis: A State-of-the-Art-Review.

Microorganisms. 2024-7-19

[4]
Current Knowledge of Enterococcal Endocarditis: A Disease Lurking in Plain Sight of Health Providers.

Pathogens. 2024-3-7

[5]
Bridging Molecular and Clinical Sciences to Achieve the Best Treatment of Endocarditis.

Microorganisms. 2023-10-21

[6]
Antibodies to coagulase of crossreact to Efb and reveal different binding of shared fibrinogen binding repeats.

Front Immunol. 2023

[7]
2023 ESC Guidelines for the management of endocarditis.

Eur Heart J. 2023-10-14

[8]
The 2023 Duke-International Society for Cardiovascular Infectious Diseases Criteria for Infective Endocarditis: Updating the Modified Duke Criteria.

Clin Infect Dis. 2023-8-22

[9]
Fibrinogen γ' promotes host survival during Staphylococcus aureus septicemia in mice.

J Thromb Haemost. 2023-8

[10]
Neutrophils Protect Against Endocarditis Progression Independent of Extracellular Trap Release.

Arterioscler Thromb Vasc Biol. 2023-2

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