Omentin-1 levels in patients with premature coronary artery disease, metabolic syndrome and healthy controls. Short communication

Stejskal, David; Václavík, J.; Smékal, Aleš; Svobodová, Gabriela; Richterova, Radmila; Švesták, Marek

doi:10.5507/bp.2016.019

Cited by 18 publications

(15 citation statements)

References 16 publications

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“…To our knowledge, our group is the first to assess omentin-1 levels in "young" patients with premature manifestations of atherosclerosis [11]. The results are in accordance with studies in older patients.…”

Section: Discussionsupporting

confidence: 89%

Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls

et al. 2019

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Section: Discussionsupporting

confidence: 89%

Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls

et al. 2019

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“… 4 Inflammation is caused by several hormones like proteins called adipokines, released from adipose tissues, which now, considered as main endocrine tissue of the body. 5 Omentin-1 is a recently identified, visceral adipose tissue derived adipokine consists of 295 amino acids, coded by gene located at chromosome 1q 21-23. 6 , 7 Omentin-1 is reported to be highly expressed in epicardial adipose tissue (EAT) around the heart and coronary arteries.…”

Section: Introductionmentioning

confidence: 99%

Association of single Nucleotide Missence Polymorphism Val109Aspof Omentin-1 gene and coronary artery disease in Pakistani population: Multicenter study

2017

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Background & Objective:Coronary artery disease (CAD) is a most important cause of morbidity and mortality worldwide as well as in Pakistan. Recent studies have shown that the combination of obesity, insulin resistance and fluctuation in circulating adipocytokines levels is associated with the pathogenesis of coronary artery disease. Omentin-1 is recently found adipocytokine that is highly expressed in visceral adipose tissue. It has anti- inflammatory properties and is negatively correlated with ischemic heart disease. Therefore, this study was designed to investigate the relationship between omentin-1 Val109Asp polymorphism and CAD in Pakistani population.Methods:A total of 350 subjects were included in the study. Two hundred fifty were diagnosed with coronary artery disease while 100 served as healthy controls. PCR-RFLP was performed at Dr. A Q. Khan Institute of Biotechnology (KIBGE) to analyze Val109Asp polymorphism. In this, case control study SPSS software version 16 (Chicago, IL, USA) was used for data analysis. Continuous variables and categorical variables were presented as mean±SD or in percentage. Independent sample test and chi-square test was performed to compare the differences in means between cases and controls. Genotype distribution was analyzed by chi-square test and results were presented as percentage and frequency. Multivarible regression analysis indicated that Val109Asp SNP might be an independent risk factor for CAD susceptibility after adjustment for some well- known CAD risk factors including age, gender, body mass index, smoking, hypertension, diabetes mellitus and lipid abnormalities. There was estimation of odd ratios (OR) and 95% confidence intervals (CIs) to determine the correlation between genotypes and the risk of CAD. (p> 0.05). Genotype frequencies were compared by Chi-square test.Results:There was prevalence of Omentin-1 Val109Asp polymorphism in both case and control groups. However, Val/Asp (heterozygous mutant) genotype was detected more frequently in patients with CAD, OR(95%)=1.921; CI=1.173-3.1469 in comparison of Asp/Asp and Val/Val genotypes.Conclusion:Individuals having Val/Asp heterozygous gemotype of omentin-1 gene polymorphism are at more risk of developing CAD in Pakistani population, further studies are required in different populations and ethnicities to confirm our findings.

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“…Arterial calcification is positively associated with visceral adiposity, but the mechanisms remain unclear. Several experimental studies demonstrated the protective role of omentin-1 in the regulation of atherogenesis [182]. This study demonstrated that recombinant human omentin-1 could induce OPG and inhibit RANKL production in primary mouse osteoblasts and calcifying vascular smooth muscle cells (CVSMs) in vitro, and adenovirus-mediated over-expression of human omentin-1 in OPG -/mice could ameliorate bone loss and arterial calcification in vivo.…”

Section: Omentin-1 Attenuates Arterial Calcification and Bone Lossmentioning

confidence: 74%

Vascular Calcification, Atherosclerosis and Bone Loss (Osteoporosis): New Pathophysiological Mechanisms and Future Perspectives for Pharmacological Therapy

2016

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Vascular calcification or ectopic mineralization in blood vessels is an active, cell-regulated process, increasingly recognized as a general cardiovascular risk factor. Ectopic artery mineralization is frequently accompanied by decreased bone mineral density or disturbed bone turnover and development of the osteoporosis. The latest data support the correlation of osteoporosis and atherosclerosis, indicating the parallel progression of two tissue destruction processes with increased fatal and nonfatal coronary events, as well as a higher fracture risk. Patients with osteoporosis, have a higher risk of cardiovascular diseases than subjects with normal bone. Many proteins responsible for bone formation and resorption have been identified in the arterial wall. Vascular calcification includes mostly osteogenic and, to a lesser extent chondrogenic differentiation of osteoblasts and osteoclast-like cells. It has been shown that many of the regulators of bone formation and resorption some bone structural proteins, such as osteoprotegerin (OPG), receptor activator of nuclear factor-κB ligand (RANKL) are also expressed in the atherosclerotic plaque. When RANKL binds to RANK, osteoclasts are activated and bone resorption occurs and processes of vascular calcification become also activated. OPG, protein homologue to receptor activator of nuclear factor-κB (RANK), can bind to RANKL, blocking the binding of RANKL to RANK, that results in inhibition of differentiation of preosteoclasts to mature osteoclasts, lower osteoclast capacity for resorption of bone mineral matrix, and development vascular calcification. The latest data supports that cathepsin K, a cysteine protease, can efficiently degrade type I and II collagen, both of which are major matrix components of the bone and atherosclerotic plaque. These findings further underscore the potential of cathepsin K as a target for novel molecules to treat osteoporosis and atherosclerosis. Thus, the discovery of the cytokine RANKL-RANK-OPG system and significant role of the cathepsin K in the process of bone remodeling, vascular calcification and atherosclerosis has made progress in understanding the mechanisms of disease development and possibly to develop new dual therapies. New therapies for osteoporosis and atherosclerosis that may potentially improve or augment existing treatments include the recently approved anti-receptor activator of NF-κB-ligand monoclonal antibody fms (denosumab) and the cathepsin K inhibitor odanacatib, presently in the late stage of clinical development.

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Omentin-1 levels in patients with premature coronary artery disease, metabolic syndrome and healthy controls. Short communication

Cited by 18 publications

References 16 publications

Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls

Plasma levels and leucocyte RNA expression of adipokines in young patients with coronary artery disease, in metabolic syndrome and healthy controls

Association of single Nucleotide Missence Polymorphism Val109Aspof Omentin-1 gene and coronary artery disease in Pakistani population: Multicenter study

Vascular Calcification, Atherosclerosis and Bone Loss (Osteoporosis): New Pathophysiological Mechanisms and Future Perspectives for Pharmacological Therapy

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