Monocytes in Acute Coronary Syndromes

Abstract

Abstract-The aim of this overview is to summarize the available data on the involvement of monocytes in the pathological processes related to the development of acute coronary syndromes and the recovery of damaged areas, the prevention of excessive inflammatory and procoagulant response, and the restoration of microcirculation (angiogenesis) Key Words: monocyte Ⅲ acute coronary syndromes Ⅲ myocardial infarction M acrophage infiltration is the initial step toward atherosclerotic plaque formation. 1 Consequent apoptosis or death of macrophages is largely responsible for necrotic core generation in the plaque, and the progressive accumulation of free cholesterol results in expansion of the necrotic core. This is perhaps a simplification, because plaque destabilization is a complex process and includes an unbalanced generation of inflammatory cytokines, as well as angiogenic and growth factors promoting pathological plaque neovascularization and matrix metalloproteinases (MMPs) digesting various proteins of extracellular matrix and ultimately resulting in the rupture of the fibrous cap of the plaque leading to intracoronary thrombus formation. 2 Although the mechanisms of plaque destabilization can be mainly attributed to the processes taken places inside the plaque, circulating peripheral blood monocytes are able to generate and secrete mediators of all the major factors involved in plaque destabilization, including inflammation, matrix degradation, and thrombogenesis (supplemental Table I, available online at http://atvb.ahajournals. org). Also, certain monocyte subpopulations possess potent in vitro angiogenic properties and constitute the main part of so-called endothelial progenitor cells (EPCs). 3 The apparent "success" of myocardial infarction (MI) treatment after restoration of effective perfusion ultimately depends on the recovery of necrotic areas (ie, removal of dead cells, granulation tissue formation, etc), the prevention of excessive inflammatory and procoagulant response(s), the restoration of microcirculation (angiogenesis), and the prevention of further growth of atherosclerotic plaque (and their stability)..Monocytes are actively involved in all of these processes, and the aim of this overview is to summarize the available data on the involvement of monocytes in the pathological processes related to acute coronary syndrome (ACS). In this article, we put an emphasis on circulating monocytes rather than on their follow-on cells, the macrophages. The role of the latter (ie, macrophages) in ACS has recently been reviewed. 4 A brief overview of monocyte counts in total blood from patients presenting with acute MI is provided in the supplemental Appendix. Monocyte ActivationBefore their involvement in the pathogenesis of ACS, monocytes are undergoing phenotypic transformation, leading to their activation. CD14, which is monocyte endotoxin receptor-together with toll-like receptors (TLR)-bind lipopolysaccharides (LPS) evoking monocyte activation, and the interaction between leukocytes and endothelium ...

Distribution of theIL-1RN,IL-6,IL-10,INF-γ, andTNF-αGene Polymorphisms in the Mexican Population

“…Both phases are characterized by increased blood flow and vascular permeability along with the accumulation of fluid, leukocytes, and inflammatory mediators, such as cytokines (Tedgui and Mallat, 2006;Shantsila and Lip, 2009). Cytokines are a group of cell-derived polypeptides that, to a large extent, orchestrate the inflammatory response.…”

“…In addition, they are pleiotropic molecules that elicit their effects locally or systemically in an autocrine or paracrine manner (Tedgui and Mallat, 2006). On the other hand, cytokines are involved in extensive networks that involve synergistic as well as antagonistic interactions and exhibit both negative and positive regulation effects on various target cells (Feghali and Wright, 1997;Tedgui and Mallat, 2006;Shantsila and Lip, 2009;). Data from several studies support the role of cytokines, such as the antagonist receptor of interleukin 1 (IL-1ra), interleukin-6 (IL-6), interleukin-10 (IL-10), interferon-gamma (INF-g), tumor necrosis factor-alpha (TNF-a), and transforming growth factor, in the acute inflammatory process (Feghali and Wright, 1997;Tedgui and Mallat, 2006;Shantsila and Lip, 2009).…”

Citokin 's profile of mononuclearsat patients by myocardialin farction, complicated cardiacinsufficiencycitokin 's profile of mononuclearsat patients by myocardialin farction, complicated cardiacinsufficiency

“…Нині участь мононуклеарних клітин (лімфо-цитів, моноцитів/макрофагів) у патогенезі атеросклерозу є доведеною [17]. Інфільтрація макрофагами -це початковий етап форму-вання атеросклеротичної бляшки.…”

Association of Toll-Like Receptor 4 on Human Monocyte Subsets and Vulnerability Characteristics of Coronary Plaque as Assessed by 64-Slice Multidetector Computed Tomography

“…The discovery that monocytes comprise distinct subsets in humans suggests a specialization of function and has stimulated interest in approaches that discriminate between "harmful" and "beneficial" subsets. [4][5][6][7] In terms of the relationship between monocyte subsets and coronary plaque instability, we previously showed by optical coherence tomography that upregulation of CD14 + CD16 + monocytes was associated with both plaque fibrous cap thickness 8 and plaque rupture 9 in patients with unstable angina pectoris. These >1.5 mg/dL) (n=19), because they could not undergo MDCT.…”