Integrating Mechanisms in Thrombotic Peripheral Arterial Disease

被引:8
作者
Nagy, Magdolna [1 ]
van der Meijden, Paola E. J. [1 ,2 ]
Glunz, Julia [3 ]
Schurgers, Leon [1 ]
Lutgens, Esther [4 ,5 ,6 ]
ten Cate, Hugo [1 ,2 ,7 ,8 ]
Heitmeier, Stefan [3 ]
Spronk, Henri M. H. [1 ,2 ,7 ]
机构
[1] Maastricht Univ, Cardiovasc Res Inst Maastricht, Dept Biochem, NL-6229 ER Maastricht, Netherlands
[2] Maastricht Univ, Thrombosis Expertise Ctr, Heart & Vasc Ctr, Med Ctr, NL-6229 HX Maastricht, Netherlands
[3] Bayer AG, Cardiovasc Res, D-42117 Wuppertal, Germany
[4] German Ctr Cardiovasc Res DZHK, Partner Site Munich Heart Alliance, D-10785 Munich, Germany
[5] Ludwig Maximilians Univ Munchen, Inst Cardiovasc Prevent IPEK, D-80539 Munich, Germany
[6] Mayo Clin, Dept Cardiovasc Med, Expt Cardiovasc Immunol Lab, Rochester, MN 55902 USA
[7] Maastricht Univ, Dept Internal Med, Med Ctr, NL-6229 HX Maastricht, Netherlands
[8] Gutenberg Univ Mainz, Ctr Thrombosis & Hemostasis, D-55122 Mainz, Germany
关键词
peripheral artery disease; coagulation; thrombosis; atherosclerosis; NEUTROPHIL EXTRACELLULAR TRAPS; ATHEROSCLEROTIC PLAQUE PROGRESSION; PROTEASE-ACTIVATED RECEPTORS; RED-BLOOD-CELLS; PLATELET ACTIVATION; CD40; LIGAND; TISSUE FACTOR; MATRIX METALLOPROTEINASE-2; PLASMA-PROTEIN; RISK-FACTORS;
D O I
10.3390/ph15111428
中图分类号
R914 [药物化学];
学科分类号
100701 ;
摘要
Peripheral arterial disease (PAD), a manifestation of systemic atherosclerosis, is underdiagnosed in the general population. Despite the extensive research performed to unravel its pathophysiology, inadequate knowledge exists, thus preventing the development of new treatments. This review aims to highlight the essential elements of atherosclerosis contributing to the pathophysiology of PAD. Furthermore, emphasis will be placed on the role of thrombo-inflammation, with particular focus on platelet and coagulation activation as well as cell-cell interactions. Additional insight will be then discussed to reveal the contribution of hypercoagulability to the development of vascular diseases such as PAD. Lastly, the current antithrombotic treatments will be discussed, and light will be shed on promising new targets aiming to aid the development of new treatments.
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页数:16
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共 120 条
[1]   Endothelial Cell Heterogeneity [J].
Aird, William C. .
COLD SPRING HARBOR PERSPECTIVES IN MEDICINE, 2012, 2 (01)
[2]   Conflicting vascular and metabolic impact of the IL-33/sST2 axis [J].
Altara, Raffaele ;
Ghali, Rana ;
Mallat, Ziad ;
Cataliotti, Alessandro ;
Booz, George W. ;
Zouein, Fouad A. .
CARDIOVASCULAR RESEARCH, 2018, 114 (12) :1578-1594
[3]   CD40L stabilizes arterial thrombi by a β3 integrin-dependent mechanism [J].
André, P ;
Prasad, KSS ;
Denis, CV ;
He, M ;
Papalia, JM ;
Hynes, RO ;
Phillips, DR ;
Wagner, DD .
NATURE MEDICINE, 2002, 8 (03) :247-252
[4]   Platelet regulation of myeloid suppressor of cytokine signaling 3 accelerates atherosclerosis [J].
Barrett, Tessa J. ;
Schlegel, Martin ;
Zhou, Felix ;
Gorenchtein, Mike ;
Bolstorff, Jennifer ;
Moore, Kathryn J. ;
Fisher, Edward A. ;
Berger, Jeffrey S. .
SCIENCE TRANSLATIONAL MEDICINE, 2019, 11 (517)
[5]   Pregnancy-associated plasma protein a as a marker of acute coronary syndromes [J].
Bayes-Genis, A ;
Conover, CA ;
Overgaard, MT ;
Bailey, KR ;
Christiansen, M ;
Holmes, DR ;
Virmani, R ;
Oxvig, C ;
Schwartz, RS .
NEW ENGLAND JOURNAL OF MEDICINE, 2001, 345 (14) :1022-1029
[6]   Melagatran reduces advanced atherosclerotic lesion size and may promote plaque stability in apolipoprotein E-deficient mice [J].
Bea, Florian ;
Kreuzer, Joerg ;
Preusch, Michael ;
Schaab, Sandra ;
Isermann, Berend ;
Rosenfeld, Michael E. ;
Katus, Hugo ;
Blessing, Erwin .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2006, 26 (12) :2787-2792
[7]   The small GTPase Rap1b regrulates the cross talk between platelet integrin α2β1 and integrin αIIbβ3 [J].
Bernardi, B ;
Guidetti, GF ;
Campus, F ;
Crittenden, JR ;
Graybiel, AM ;
Balduini, C ;
Torti, M .
BLOOD, 2006, 107 (07) :2728-2735
[8]  
Bhatt D L, 2001, J Invasive Cardiol, V13, P767
[9]   Clopidogrel and aspirin versus aspirin alone for the prevention of atherothrombotic events [J].
Bhatt, DL ;
Fox, KAA ;
Hacke, W ;
Berger, PB ;
Black, HR ;
Boden, WE ;
Cacoub, P ;
Cohen, EA ;
Creager, MA ;
Easton, JD ;
Flather, MD ;
Haffner, SM ;
Hamm, CW ;
Hankey, GJ ;
Johnston, SC ;
Mak, KH ;
Mas, JL ;
Montalescot, G ;
Pearson, TA ;
Steg, PG ;
Steinhubl, SR ;
Weber, MA ;
Brennan, DM ;
Fabry-Ribaudo, L ;
Booth, J ;
Topol, EJ ;
Frye, RL ;
Amarenco, P ;
Brass, LM ;
Buyse, M ;
Cohen, LS ;
DeMets, DL ;
Fuster, V ;
Hart, RG ;
Marler, JR ;
McCarthy, C ;
Schoemig, A ;
Lincoff, AM ;
Brener, SJ ;
Sila, CA ;
Albuquerque, A ;
Aroutiounov, G ;
Artemiev, D ;
Atkeson, BG ;
Bartel, T ;
Basart, DCG ;
Lima, AB ;
Belli, G ;
Bordalo e Sa, AL ;
Bosch, X .
NEW ENGLAND JOURNAL OF MEDICINE, 2006, 354 (16) :1706-1717
[10]   Antiplatelet therapy in acute coronary syndromes: focus on ticagrelor [J].
Birkeland, Kade ;
Parra, David ;
Rosenstein, Robert .
JOURNAL OF BLOOD MEDICINE, 2010, 1 :197-219