Role of Epicardial Adipose Tissue in Atherosclerosis and Coronary Artery Disease
Author:
Gianluca Iacobellis, M.D., Ph.D.
The reason for the growing scientific interest into the fat is the widely-accepted acknowledgement that adipose tissue is not a silent organ, but a very active source of multiple bioactive cytokines, called adipokines. The adipocyte, mini-organ within this neglected organ, sends outputs (adipokines) and accepts inputs (nuclear receptors). The adipose tissue communicates with almost all other organs through endocrine, paracrine, and also autocrine interactions. Hence, both systemic and local regulations of internal organs' function and morphology have been recently attributed to the adipose tissue.
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Asymmetric Dimethylarginine and Coronary Artery Disease
Authors:
Asife Sahinarslan, M.D., and Atiye Cengel, M.D.
Endothelium, the inner surface of the vasculature, is responsible for maintenance of the normal vascular functions, like control of vascular tonus, homeostasis, and inflammation, through secretion of vasoactive molecules. The most important molecule which regulates the functions of endothelium is nitric oxide (NO). NO is synthesized from L-arginine by the help of nitric oxide synthase (NOS).
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Carbamylated LDL Induces Monocyte Adhesion to Endothelial Cells
Authors:
Alexei G. Basnakian, M.D., Ph.D.
Our recent study [1] was undertaken to determine whether monocyte adhesion to endothelial cells can be induced by carbamylated LDL (cLDL) and to identify the adhesion molecules involved in this process. We utilized U937 monocyte cells and human coronary artery endothelial cells (HCAEC), commonly used for studies of monocyte adhesion. We demonstrated that cLDL induces intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) on endothelial cells, and the role of these adhesion molecules in the attraction of monocytes in vitro.
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The Safety of Statin-Niacin Combination Therapy
Authors: Alawi A. Alsheikh-Ali, M.D. and Richard H. Karas, M.D., Ph.D.
Current national guidelines advocate aggressive lipid goals for the prevention of cardiovascular disease [1,2]. In addition to setting low-density lipoprotein cholesterol (LDL-C) as the primary target, they recognize high-density lipoprotein cholesterol (HDL-C) as an independent risk factor, and encourage the use of HDL-C raising therapies in high-risk patients [1,2]. Nonetheless, there remains gross under-treatment of HDL-C in high-risk patients. While several factors may contribute to the underutilization of HDL-C raising therapies in appropriate patients, concerns about the safety of combining a statin with niacin may be partly responsible.
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Endotoxin Induces Toll-Like Receptor 4 Expression in Vascular Cells: A Novel
Mechanism Involved in Vascular Inflammation
Authors: Feng-Yen Lin, Ph.D. and Shing-Jong Lin, M.D., PhD.
Toll-like receptors (TLRs) are type I transmembrane receptors that expressed on the cell
membrane after lipopolysaccharide (LPS) stimulation [1]. TLRs are critical for the induction of
downstream signals in atherogenesis during endotoxin-mediated vascular disturbances. Previous
studies have demonstrated that TLR4 is abundantly expressed in failing myocardium [2], and in
macrophages infiltrating lipid-rich atherosclerotic lesions [3]. Moreover, an association between
the functional expression of TLR4 and the subsequent intimal hyperplasia has recently been
described [4]. TLR4 mediates and regulates LPS-induced proinflammatory activation in vascular
smooth muscle cells (VSMCs) [5].
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Will Genomics Provide New Insights into the Diversity of Plaque Macrophages?
Authors: Andrew C. Newby, M.A., Ph.D., Graciela B. Sala-Newby, Ph.D., Anita C. Thomas, and Jason L. Johnson, Ph.D.
Macrophages are found in atherosclerotic plaques at all stages [1]. Once low density lipoprotein (LDL) enters and becomes trapped in the vascular intima, monocytes are recruited from the circulation, differentiate to macrophages, and accumulate cholesteryl esters to become foam cells [2,3]. Early fatty streaks consist of foamy macrophages and only a few foamy smooth muscle cells (SMCs) and therefore appear highly inflammatory. Nevertheless fatty streaks do not cause symptoms, are covered by an intact endothelium, and appear completely reversible [4].
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Metabolic Syndrome, Cardiovascular Disease, and Mitochondrial Function: Molecular Replacement and Antioxidant Supplements to Prevent Membrane Oxidation and Restore Mitochondrial Function
Authors: Garth L. Nicolson, PhD
One of the central defects in metabolic syndrome (MS) and its associated diseases (type-2 diabetes, vascular inflammation, atherosclerosis, among other diseases) as well as fatiguing illnesses is excess cellular oxidative stress. Oxidative stress affects many organ systems, including pancreatic beta cells, nerve cells, immune cells, and it generally affects the vascular system. Oxidative damage to membranes results in reduced efficiency of the mitochondrial electron transport chain, the main source of energy in our cells. Recent evidence indicates that reduced mitochondrial function caused by membrane oxidation is related to fatigue, a complaint in MS and cardiovascular disease (CVD) and the major complaint in fatiguing illnesses. Lipid replacement therapy administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial membrane function, and reduce fatigue in a variety of clinical conditions.
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Insulin Secretion and Insulin Resistance in Newly Diagnosed, Drug Naive
Prediabetes and Type 2 Diabetes Patients With/Without Metabolic Syndrome
Authors: Sang Youl Rhee, M.D., Suk Chon, M.D., Ph.D., Seungjoon Oh, M.D., Ph.D., Sung Woon Kim, M.D., Ph.D., Jin-Woo Kim, M.D., Ph.D.,
Young Seol Kim, M.D., Ph.D., and Jeong-taek Woo, M.D., Ph.D.
The pathogenesis of diabetes is complicated by several metabolism-related problems. In
particular, a deterioration in insulin secretion and an aggravation of insulin resistance
are known to be essentials in the primary pathogenesis of type 2 diabetes mellitus (DM)
[1]. In terms of insulin resistance, type 2 DM and metabolic syndrome (MS) are closely
related. The Botnia study showed that 84% of men and 78% of women with type 2 DM
had accompanying MS. For patients with prediabetes, 64% of men and 42% of women
had MS, and for normal glucose tolerance (NGT) groups, only 15% of men and 10% of
women had MS [2]. However, not all type 2 DM patients have MS and neither do all
MS patients have accompanying type 2 DM.
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Ghrelin has Novel Vascular Actions that Mimic Insulin-stimulated Production of Nitric Oxide
Authors: Micaela Iantorno, M.D. and Michael J. Quon, M.D., Ph.D.
Ghrelin is a 28 amino acid peptide hormone secreted from X/A-like cells in the oxyntic mucosa of the stomach that has central actions to stimulate growth hormone release and orexigenesis [1]. The cognate receptor for ghrelin, GHSR-1a, is a 7-transmembrane G-protein coupled receptor that mediates most of the biological actions of ghrelin [2]. The principal physiological function of GHSR-1a was previously thought to be stimulation of growth hormone release from pituitary. However, GHSR-1a is expressed in many cell types including cardiomyocytes, myocardium, vascular endothelium, and monocytes raising the possibility that ghrelin may also have physiological actions in peripheral tissues.
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Obesity and Thrombosis: Role of Inflammation and Insulin Resistance Per Se
Authors: Giovanni Davì, M.D., and Francesca Santilli, M.D.
Insulin resistance is an independent risk factor for coronary artery disease, but the mechanisms predisposing insulin-resistant individuals to atherothrombosis are poorly understood [1]. Coronary artery disease has been related to chronic, subclinical inflammation, as indicated by elevated circulating levels of inflammatory proteins [2].
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Metabolic Syndrome: Available Evidence Urges To Action the Society and Each of Us
Author:
Teodoro Marotta, M.D., Ph.D.
Three new prospective, general-population-based studies published in the first months of this year [1-3], in which data of 24,800; 24,100; and 13,300 person-years, respectively, have been analyzed, highlight the link of metabolic syndrome (MS) with total [1,2] and cardiovascular [1-3] mortality. In the smallest of these studies [3], indeed, the association of cardiovascular mortality with MS was not stronger than that with the single components of the syndrome.
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Carotid Intima-Media Thickness in Patients Referred for Endarterectomy
Authors: Mario De Michele, M.D. and M. Gene Bond, Ph.D.
Over the last two decades, B-mode ultrasound has been increasingly used to detect both early and advanced carotid atherosclerosis. In clinical practice, duplex ultrasound allows accurate measurement of the degree of lumen stenosis, which is the parameter used to select patients for carotid surgery. On the other hand, epidemiological studies have focused on the evaluation of carotid intima-media thickness (IMT), a valid and reliable measure of arterial wall atherosclerotic disease [1].
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Carotid Atherosclerosis in "White-Coat" and "Masked" Hypertension
Authors:
Azusa Hara, Takayoshi Ohkubo
M.D., Ph.D.
, and Yutaka Imai, M.D., Ph.D.
The utility of measurement of blood pressure (BP) outside medical settings, such as home BP (HBP) or ambulatory BP (ABP) measurement has been recognized, and the practice has been adopted widely [1,2]. The Ohasama study has provided clear evidence on the superiority of HBP measurement versus casual or clinic BP (CBP) measurement to predict the risk of events [3,4]. Some studies also have shown that the target organ damage of hypertension correlates more closely with HBP values than with CBP values [5]. These beneficial characteristics of HBP measurement may be derived from an increase in the number of measurements taken [3,4].
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Dimethylated L-Arginine Analogs and Atherogenesis
Authors: Andrzej Surdacki, M.D.
Asymmetric N G ,N G -dimethyl-L-arginine (ADMA), an endogenous competitive inhibitor of nitric oxide (NO) synthesis, is formed by methylation of the guanidine nitrogens of arginine residues within proteins through the action of S-adenosylmethionine-dependent protein arginine N-methyltransferases (PRMTs) type I (PRMTs-I), which catalyze formation of ADMA and NG-monomethyl-L-arginine (L-NMMA) [1,2]. In contrast, symmetric N G ,N' G -dimethyl-L-arginine (SDMA) (a stereoisomer of ADMA) and L-NMMA are products of PRMTs type II (PRMTs-II) [1,2].
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Cholesterol-Induced Membrane Microvesicles: Novel Contributors to Atherothrombosis
Authors: Ming-Lin Liu, M.D., Ph.D.
Microvesicles (MV), also known as microparticles, are small membranous structures that are released from cells upon activation or during apoptosis [1-5]. Many cell types have been shown to release MVs, including circulating platelets, leukocytes, and erythrocytes, as well as cells of the vascular wall, mainly endothelium, macrophages, and smooth muscle cells [1-5]. MVs can be detected by flow cytometry, electromicroscopy, or ELISA with Annexin V-coated plates [2]. Of these methods, flow cytometry has been the most commonly used, owing to its wide availability and its capacity for individually characterizing large numbers of MVs.
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