A link between inflammation and thrombosis in atherosclerotic cardiovascular diseases: Clinical and therapeutic implications

被引:77
作者
Oikonomou, Evangelos [1 ]
Leopoulou, Marianna [1 ]
Theofilis, Panagiotis [1 ]
Antonopoulos, Alexios S. [1 ]
Siasos, Gerasimos [1 ]
Latsios, George [1 ]
Mystakidi, Vasiliki Chara [1 ]
Antoniades, Charalambos [2 ]
Tousoulis, Dimitris [1 ]
机构
[1] Natl & Kapodistrian Univ Athens, Hippokration Hosp, Dept Cardiol 1, Med Sch, Athens, Greece
[2] Univ Oxford, Radcliffe Dept Med, Div Cardiovasc Med, Oxford, England
关键词
Atherosclerosis; Cardiovascular disease; Cytokines; Inflammation; Thrombosis; Platelets; C-REACTIVE PROTEIN; CORONARY-ARTERY-DISEASE; VON-WILLEBRAND-FACTOR; ST-SEGMENT ELEVATION; NEUTROPHIL EXTRACELLULAR TRAPS; ACUTE MYOCARDIAL-INFARCTION; MEAN PLATELET VOLUME; SOLUBLE CD40 LIGAND; ENDOTHELIAL-CELLS; TISSUE FACTOR;
D O I
10.1016/j.atherosclerosis.2020.07.027
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The association between thrombosis and acute coronary syndromes is well established. Inflammation and activation of innate and adaptive immunity are another important factor implicated in atherosclerosis. However, the exact interactions between thrombosis and inflammation in atherosclerosis are less well understood. Accumulating data suggest a firm interaction between these two key pathophysiologic processes. Pro-inflammatory cytokines, such as tumor necrosis factor alpha, interleukin-6 and interleukin-1, have been implicated in the thrombotic cascade following plaque rupture and myocardial infarction. Furthermore, cell adhesion molecules accelerate not only atheromatosis but also thrombosis formation while activated platelets are able to trigger leukocyte adhesion and accumulation. Additionally, tissue factor, thrombin, and activated coagulation factors induce the release of pro-inflammatory cytokines such as prostaglandin and C reactive protein, which may further induce von Willebrand factor secretion. Treatments targeting immune activation (i.e. interleukin-1 inhibitors, colchicine, statins, etc.) may also beneficially modulate platelet activation while common antithrombotic therapies appear to attenuate the inflammatory process. Taken together in the context of cardiovascular diseases, thrombosis and inflammation should be studied and managed as a common entity under the concept of thrombo-inflammation.
引用
收藏
页码:16 / 26
页数:11
相关论文
共 182 条
[51]   Regulation of tumor necrosis factor receptor-1 and the IKK-NF-κB pathway by LDL receptor-related protein explains the antiinflammatory activity of this receptor [J].
Gaultier, Alban ;
Arandjelovic, Sanja ;
Niessen, Sherry ;
Overton, Cheryl D. ;
Linton, MacRae F. ;
Fazio, Sergio ;
Campana, W. Marie ;
Cravatt, Benjamin F., III ;
Gonias, Steven L. .
BLOOD, 2008, 111 (11) :5316-5325
[52]   Effect of CC Chemokine Receptor 2 CCR2 Blockade on Serum C-Reactive Protein in Individuals at Atherosclerotic Risk and With a Single Nucleotide Polymorphism of the Monocyte Chemoattractant Protein-1 Promoter Region [J].
Gilbert, Jim ;
Lekstrom-Himes, Julie ;
Donaldson, Debra ;
Lee, Yih ;
Hu, Mingxiu ;
Xu, Jing ;
Wyant, Tim ;
Davidson, Michael .
AMERICAN JOURNAL OF CARDIOLOGY, 2011, 107 (06) :906-911
[53]   Platelet reactivity in response to loading dose of atorvastatin or rosuvastatin in patients with stable coronary disease before percutaneous coronary intervention: The STATIPLAT randomized study [J].
Godino, Cosmo ;
Pavon, Anna Giulia ;
Mangieri, Antonio ;
Salerno, Anna ;
Cera, Michela ;
Monello, Alberto ;
Chieffo, Alaide ;
Magni, Valeria ;
Cappelletti, Alberto ;
Margonato, Alberto ;
Colombo, Antonio .
CLINICAL CARDIOLOGY, 2017, 40 (08) :605-611
[54]   NLRP3 Inflammasome and the IL-1 Pathway in Atherosclerosis [J].
Grebe, Alena ;
Hoss, Florian ;
Latz, Eicke .
CIRCULATION RESEARCH, 2018, 122 (12) :1722-1740
[55]   Leukocyte-versus microparticle-mediated tissue factor transfer during arteriolar thrombus development [J].
Gross, PL ;
Furie, BC ;
Merrill-Skoloff, G ;
Chou, J ;
Furie, B .
JOURNAL OF LEUKOCYTE BIOLOGY, 2005, 78 (06) :1318-1326
[56]   Rivaroxaban, a novel oral anticoagulant, attenuates atherosclerotic plaque progression and destabilization in ApoE-deficient mice [J].
Hara, Tomoya ;
Fukuda, Daiju ;
Tanaka, Kimie ;
Higashikuni, Yasutomi ;
Hirata, Yoichiro ;
Nishimoto, Sachiko ;
Yagi, Shusuke ;
Yamada, Hirotsugu ;
Soeki, Takeshi ;
Wakatsuki, Tetsuzo ;
Shimabukuro, Michio ;
Sata, Masataka .
ATHEROSCLEROSIS, 2015, 242 (02) :639-646
[57]   Inflammation in acute coronary syndrome: Expression of TLR2 mRNA is increased in platelets of patients with ACS [J].
Heger, Lukas Andreas ;
Hortmann, Marcus ;
Albrecht, Madlin ;
Colberg, Christian ;
Peter, Karlheinz ;
Witsch, Thilo ;
Stallmann, Daniela ;
Zirlik, Andreas ;
Bode, Christoph ;
Duerschmied, Daniel ;
Ahrens, Ingo .
PLOS ONE, 2019, 14 (10)
[58]   Nitric oxide activates diverse signaling pathways to regulate gene expression [J].
Hemish, J ;
Nakaya, N ;
Mittal, V ;
Enikolopov, G .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (43) :42321-42329
[59]   Effect of interleukin-6 inhibition on coronary microvascular and endothelial function in myocardial infarction [J].
Holte, Espen ;
Kleveland, Ola ;
Ueland, Thor ;
Kunszt, Gabor ;
Bratlie, Marte ;
Broch, Kaspar ;
Michelsen, Annika E. ;
Bendz, Bjorn ;
Amundsen, Brage H. ;
Aakhus, Svend ;
Damas, Jan Kristian ;
Gullestad, Lars ;
Aukrust, Pal ;
Wiseth, Rune .
HEART, 2017, 103 (19) :1521-1527
[60]   Platelets mediate increased endothelium permeability in dengue through NLRP3-inflammasome activation [J].
Hottz, Eugenio D. ;
Lopes, Juliana F. ;
Freitas, Carla ;
Valls-de-Souza, Rogerio ;
Oliveira, Marcus F. ;
Bozza, Marcelo T. ;
Da Poian, Andrea T. ;
Weyrich, Andrew S. ;
Zimmerman, Guy A. ;
Bozza, Fernando A. ;
Bozza, Patricia T. .
BLOOD, 2013, 122 (20) :3405-3414