Circulating adhesion molecules, matrix metalloproteinase-9, plasminogen activator inhibitor-1, and myeloperoxidase in coronary artery disease patients with stable and unstable angina

Tretjakovs, Pēteris; Jurka, Antra; Bormane, Inga; Miķelsone, Indra; Elksne, K.; Krievina, Gita; Reihmane, Dace; Verbovenko, J.; Bahs, Guntis

doi:10.1016/j.cca.2011.10.009

Cited by 36 publications

(20 citation statements)

References 19 publications

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“…Mocatta et al (93) retrospectively analyzed 512 patients admitted to the hospital for myocardial infarction and 156 healthy controls and found higher MPO plasma values in patients with myocardial infarction; of interest, above-median values of MPO were independent predictors of total mortality in a follow up of 5 years. Similar findings were obtained by Tretjakovs et al (136) in patients with unstable angina compared with patients with stable angina and controls.…”

Section: Laboratory Methodologysupporting

confidence: 89%

Clinical Application of NOX Activity and Other Oxidative Biomarkers in Cardiovascular Disease: A Critical Review

Violi

Pignatelli

2015

Antioxidants & Redox Signaling

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This review will analyze the strengths and weaknesses of the current methodology to study these enzymes in human atherosclerosis with particular regard to their clinical application in several settings of cardiovascular disease. Clinical methodology and results of previous studies with regard to markers of LDL oxidation have also been reviewed as a useful background for the future development of clinical trials.

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Section: Laboratory Methodologysupporting

confidence: 89%

Clinical Application of NOX Activity and Other Oxidative Biomarkers in Cardiovascular Disease: A Critical Review

Violi

Pignatelli

2015

Antioxidants & Redox Signaling

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“…Similarly, Wainstein et al determined CAD severity using a six-tier scoring system. They defined non-significant CAD as <70% stenosis in ≥1 epicardial vessel and <50% stenosis of the left main coronary [104], whereas most studies considered >50% stenosis in an epicardial vessel to be significant disease [1,88,[92][93][94][95]98,102,103]. MPO was reported in one study not to correlate with coronary artery calcification as determined by electron beam computed tomography [107].…”

Section: Evidence For Association Between Circulating Mpo and Cadmentioning

confidence: 99%

“…Its suitability as a potential biomarker for CVD is supported by the demonstration of 30-fold higher amounts of 3-chlorotyrosine LDL present in human atherosclerotic lesions compared with that in Peroxidase activity by guaiacol oxidation [91] Plasma Sandwich ELISA [100] Serum ELISA [175] Plasma EIA [92] EDTA plasma [97] Plasma ELISA [98] Plasma ELISA [93] Serum Sandwich ELISA [96] EDTA plasma Microparticle immunoassay [101] [94] Plasma ELISA [89] Plasma ELISA [88] Serum ELISA [95] Serum Microparticle immunoassay [90] Isolated leukocytes FACS [99] EDTA plasma ELISA Studies contradicting [103] EDTA plasma ELISA [104] Heparin plasma ELISA [107] EDTA plasma Sandwich ELISA [102] Plasma Sandwich ELISA [105] Plasma ELISA Table 8. Association between MPO and MACE prediction.…”

Section: Surrogate Biomarkersmentioning

confidence: 99%

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The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

et al. 2016

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Atherosclerosis is the main pathophysiological process underlying coronary artery disease (CAD). Acute complications of atherosclerosis, such as myocardial infarction, are caused by the rupture of vulnerable atherosclerotic plaques, which are characterized by thin, highly inflamed, and collagen-poor fibrous caps. Several lines of evidence mechanistically link the heme peroxidase myeloperoxidase (MPO), inflammation as well as acute and chronic manifestations of atherosclerosis. MPO and MPO-derived oxidants have been shown to contribute to the formation of foam cells, endothelial dysfunction and apoptosis, the activation of latent matrix metalloproteinases, and the expression of tissue factor that can promote the development of vulnerable plaque. As such, detection, quantification and imaging of MPO mass and activity have become useful in cardiac risk stratification, both for disease assessment and in the identification of patients at risk of plaque rupture. This review summarizes the current knowledge about the role of MPO in CAD with a focus on its possible roles in plaque rupture and recent advances to quantify and image MPO in plasma and atherosclerotic plaques.

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“…In contrast however, MMP-3 and ApoE double knockout mice showed increased plaque size [123]. Elevated level of MMP-9 in subjects with coronary artery disease with unstable angina has also been reported [124]. Thus, although the exact role of MMPs in atherosclerosis is remains controversial, based on the aforementioned studies it can be concluded that elevated levels of MMPs, especially MMP-2 and -9 is detrimental, in that, they enhance matrix destruction and cause inflammation, which possibly results in plaque rupture.…”

Section: Role Of Proteases In Cardiometabolic Diseasesmentioning

confidence: 99%

Proteases in cardiometabolic diseases: Pathophysiology, molecular mechanisms and clinical applications

Hua

Nair

2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Cardiovascular disease is the leading cause of death in the U.S. and other developed country. Metabolic syndrome, including obesity, diabetes/insulin resistance, hypertension and dyslipidemia is major threat for public health in the modern society. It is well established that metabolic syndrome contributes to the development of cardiovascular disease collective called as cardiometabolic disease. Despite documented studies in the research field of cardiometabolic disease, the underlying mechanisms are far from clear. Proteases are enzymes that break down proteins, many of which have been implicated in various diseases including cardiac disease. Matrix metalloproteinase (MMP), calpain, cathepsin and caspase are among the major proteases involved in cardiac remodeling. Recent studies have also implicated proteases in the pathogenesis of cardiometabolic disease. Elevated expression and activities of proteases in atherosclerosis, coronary heart disease, obesity/insulin-associated heart disease as well as hypertensive heart disease have been documented. Furthermore, transgenic animals that are deficient in or overexpress proteases allow scientists to understand the causal relationship between proteases and cardiometabolic disease. Mechanistically, MMPs and cathepsins exert their effect on cardiometabolic diseases mainly through modifying the extracellular matrix. However, MMP and cathepsin are also reported to affect intracellular proteins, by which they contribute to the development of cardiometabolic diseases. On the other hand, activation of calpain and caspases has been shown to influence intracellular signaling cascade including the NF-κB and apoptosis pathways. Clinically, proteases are reported to function as biomarkers of cardiometabolic diseases. More importantly, the inhibitors of proteases are credited with beneficial cardiometabolic profile, although the exact molecular mechanisms underlying these salutary effects are still under investigation. A better understanding of the role of MMPs, cathepsins, calpains and caspases in cardiometabolic diseases process may yield novel therapeutic targets for threating or controlling these diseases.

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Circulating adhesion molecules, matrix metalloproteinase-9, plasminogen activator inhibitor-1, and myeloperoxidase in coronary artery disease patients with stable and unstable angina

Cited by 36 publications

References 19 publications

Clinical Application of NOX Activity and Other Oxidative Biomarkers in Cardiovascular Disease: A Critical Review

Clinical Application of NOX Activity and Other Oxidative Biomarkers in Cardiovascular Disease: A Critical Review

The roles of myeloperoxidase in coronary artery disease and its potential implication in plaque rupture

Proteases in cardiometabolic diseases: Pathophysiology, molecular mechanisms and clinical applications

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