Angiotensin-converting enzyme inhibition reduces monocyte chemoattractant protein-1 and tissue factor levels in patients with myocardial infarction

Soejima, Hirofumi; Ogawa, Hisao; Yasue, Hirofumi; Kaikita, Koichi; Takazoe, Keiji; Nishiyama, Koichi; Misumi, Kenji; Miyamoto, Shinzo; Yoshimura, Michihiro; Kugiyama, Kiyotaka; Nakamura, Shin; Tsuji, Ichiro

doi:10.1016/s0735-1097(99)00318-6

Cited by 108 publications

(45 citation statements)

References 43 publications

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“…Therefore, it is necessary to consider the MI models used in different studies. Consistent with the results of the experimental studies, elevated serum concentrations of several chemokines were observed in patients with MI, 33 suggesting the clinical significance of chemokines in the pathophysiology of MI.…”

Section: Takahashi Msupporting

confidence: 85%

Role of the SDF-1/CXCR4 System in Myocardial Infarction

Takahashi

2010

Circ J

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Section: Takahashi Msupporting

confidence: 85%

Role of the SDF-1/CXCR4 System in Myocardial Infarction

Takahashi

2010

Circ J

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“…48 Of particular interest is the observation that angiotensin II induces TF expression in monocytes, endothelial cells, and vascular smooth muscle cells 24,32 through the angiotensin II type I receptor (AT-I). 32 Consistently, both ACE inhibitors 49 and AT-I receptor blockers 50 reduce TF plasma activity in hypertensive patients. ACE inhibitors also reduce endotoxin-induced TF expression in monocytes, 51 suggesting a pleiotropic effect of this class of drugs.…”

Section: Cardiovascular Risk Factorsmentioning

confidence: 79%

Tissue Factor in Cardiovascular Diseases

2006

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Abstract-Tissue factor (TF), formerly known as thromboplastin, is the key initiator of the coagulation cascade; it binds factor VIIa resulting in activation of factor IX and factor X, ultimately leading to fibrin formation. TF expression and activity can be induced in endothelial cells, vascular smooth muscle cells, and monocytes by various stimuli such as cytokines, growth factors, and biogenic amines. These mediators act through diverse signal transduction mechanisms including MAP kinases, PI3-kinase, and protein kinase C. Cellular TF is present in three pools as surface, encrypted, and intracellular protein. TF can also be detected in the bloodstream, referred to as circulating or blood-borne TF. Elevated levels of TF are observed in patients with cardiovascular risk factors such as hypertension, diabetes, dyslipidemia, and smoking as well as in those with acute coronary syndromes. TF may indeed be involved in the pathogenesis of atherosclerosis by promoting thrombus formation; in addition, it can induce migration and proliferation of vascular smooth muscle cells. As a consequence, therapeutic strategies have been developed to specifically interfere with the action of TF such as antibodies against TF, site-inactivated factor VIIa, or recombinant TF pathway inhibitor.

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“…23,[33][34][35][36] In addition to lowering cholesterol levels, life-saving statin therapy attenuates the production of inflammatory cytokines and coagulant factors and decreases the expression of cell adhesion molecules by circulating monocytes in hypercholesterolemic patients. [37][38][39] Angiotensin-converting enzyme inhibitors reduce tissue factor and serum levels of monocyte chemotactic protein 1 in patients after acute MI, 40 decelerating the coagulationinflammation-thrombosis cascade. Furthermore, addition of the renin inhibitor aliskiren suppresses circulating numbers of classical monocytes and increases myocardial salvage after acute MI.…”

mentioning

confidence: 99%

Monocyte Fate in Atherosclerosis

Hilgendorf

Świrski

Robbins

2015

ATVB

170

122

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Abstract-Monocytes and their descendant macrophages are essential to the development and exacerbation of atherosclerosis, a lipid-driven inflammatory disease. Lipid-laden macrophages, known as foam cells, reside in early lesions and advanced atheromata. Our understanding of how monocytes accumulate in the growing lesion, differentiate, ingest lipids, and contribute to disease has advanced substantially over the last several years. These cells' remarkable phenotypic and functional complexity is a therapeutic opportunity: in the future, treatment and prevention of cardiovascular disease and its complications may involve specific targeting of atherogenic monocytes/macrophages and their products.

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Angiotensin-converting enzyme inhibition reduces monocyte chemoattractant protein-1 and tissue factor levels in patients with myocardial infarction

Abstract: This study demonstrated that administration of enalapril reduces the increased procoagulant activity in patients with myocardial infarction associated with inhibition of the activation and accumulation of macrophages and monocytes.

Cited by 108 publications

References 43 publications

Role of the SDF-1/CXCR4 System in Myocardial Infarction

Role of the SDF-1/CXCR4 System in Myocardial Infarction

Tissue Factor in Cardiovascular Diseases

Monocyte Fate in Atherosclerosis

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