Inflammation as a Cardiovascular Risk Factor

Willerson, James T.; Ridker, Paul M.

doi:10.1161/01.cir.0000129535.04194.38

Cited by 937 publications

(827 citation statements)

References 98 publications

(99 reference statements)

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“…It is interesting to note that in this study 100% of patients were having serum LDL-C concentration less than 160 mg/dl, which is the accepted high risk for CAD. This observation falls in accordance with findings of Willerson, who after extensive data analysis inferred that high CRP/Low LDL-C persons are at higher absolute risk than low CRP/high LDL-C persons [31]. However, it has been pointed out that CRP concentration has continuous association with the risk of coronary heart disease, ischemic stroke, vascular mortality and death from several cancers and lung diseases that are each of broadly similar size.…”

Section: Discussionsupporting

confidence: 91%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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Acute myocardial Infarction is one of the major causes of morbidity & mortality in world and atherosclerosis is the major cause of ischemic heart disease. In order to determine the better clinical marker of atherosclerosis, we estimated serum low-density lipoprotein (LDL-C) and high sensitivity C-reactive protein (hsCRP). Hundred patients of myocardial infarction and 100 controls irrespective of age and sex were studied for these parameters over a period of 2 years. The statistical analysis showed that the serum hsCRP was significantly raised in myocardial infarction cases than controls (P \ 0.01) but LDL-C was not (P [ 0.05). We conclude that the serum hsCRP has better predictive value for risk of atherosclerosis.

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Section: Discussionsupporting

confidence: 91%

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Datta¹,

Iqbal²,

Prasad³

2011

Ind J Clin Biochem

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“…Where studied, the upregulation of inflammatory mediators was linked to increased oxidative stress, impaired mitochondrial function and abnormal cholesterol metabolism [174][175][176]. Interventions targeting cholesterol metabolism or oxidative stress also ameliorated inflammation [167,[177][178][179][180][181][182]. We therefore conclude that the metabolic concept and the immunological concept are simply two views of the same process, seen from different angles.…”

Section: Low-grade Inflammation and Healthmentioning

confidence: 82%

“…Cross-sectional and prospective studies in the general population, the elderly, and centenarians have shown that mildly elevated levels of CRP and proinflammatory cytokines are associated with, or predict, atherosclerosis, myocardial infarction, stroke, depression and Alzheimer's disease, and that longevity is associated with decreased systemic inflammation [105,[167][168][169][170][171]. Here, again, polymorphisms in immune genes modulate risk, implying a pathogenetic significance for immune gene products Table 4 Interventions that have an impact on the inflammatory state Inflammatory mediators whose concentrations are reduced by weight loss and/or physical exercise [190][191][192][193][194][195][196][197][198][199][200][201][202][203][204][205][206][207] CRP, TNF-α, soluble TNF-α receptor 2, IL-6, IL-18, MCP-1, PAI-1, t-PA, soluble ICAM-1, soluble VCAM-1, P-selectin Inflammatory mediators whose concentrations are reduced by glucose-lowering drugs [186,188,[208][209][210][211][212][213][214][215][216][217] Sulphonylurea: TNF-α Metformin: CRP Glitazones: CRP, SAA, TNF-α, soluble CD40 ligand, PAI-1 Insulin: CRP, IL-1, IL-6, TNF-α, soluble ICAM-1, MCP-1, PAI-1 SAA Serum amyloid A, t-PA tissue plasminogen activator, VCAM-1 vascular cell adhesion molecule-1 [171][172]…”

Section: Low-grade Inflammation and Healthmentioning

confidence: 99%

An immune origin of type 2 diabetes?

2005

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Subclinical, low-grade systemic inflammation has been observed in patients with type 2 diabetes and in those at increased risk of the disease. This may be more than an epiphenomenon. Alleles of genes encoding immune/ inflammatory mediators are associated with the disease, and the two major environmental factors the contribute to the risk of type 2 diabetes-diet and physical activity-have a direct impact on levels of systemic immune mediators. In animal models, targeting of immune genes enhanced or suppressed the development of obesity or diabetes. Obesity is associated with the infiltration and proinflammatory activity of macrophages in adipose tissue, and immune mediators may be important regulators of insulin resistance, mitochondrial function, ectopic lipid storage and beta cell dysfunction or death. Intervention studies targeting these pathways would help to determine the contribution of an activated innate immune system to the development of type 2 diabetes.

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“…In the atherosclerotic lesion, vascular cells release a number of inflammatory cytokines, such as IL-6, IL-1, TNF-α and chemokine (C-C motif) ligand 2 (CCL2, also known as monocyte chemoattractant protein-1) [2]. The role of insulin in atherogenesis has long been a matter of debate, with many epidemiological studies [3] suggesting that hyperinsulinaemia is a strong independent risk factor for a cardiovascular event [4,5].…”

Section: Introductionmentioning

confidence: 99%

Increased expression of CCAAT/enhancer binding protein-β and -δ and monocyte chemoattractant protein-1 genes in aortas from hyperinsulinaemic rats

et al. 2006

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Aims/hypothesis We evaluated whether hyperinsulinaemia stimulates the expression of transcription factor CCAAT/ enhancer binding protein (C/EBP)-β and C/EBP-δ and leads to the induction of the chemokine (C-C motif) ligand 2 gene (Ccl2, also known as MCP-1) expression in aortas. Methods Hyperinsulinaemia was induced by feeding rats a high-fructose diet. CCL2 production was analysed by ELISA. The expression of Ccl2, Cebpb and Cebpd mRNAs was investigated by quantitative RT-PCR. The binding of C/EBP-β to Ccl2 was assessed by chromatin immunoprecipitation (ChIP) assay. Results Insulin at a concentration of 10 nmol/l significantly stimulated the expression of Cebpb,Cebpd and Ccl2 mRNAs, depending on activation of phosphatidylinositol 3-kinase (PI3K) in cultured vascular smooth muscle cells. The knockdown of C/EBP-β with siRNA abolished the insulin-induced Ccl2 mRNA expression. In the aortas from fructose-fed rats, the levels of phosphorylation of Akt/protein kinase B, a downstream effector of PI3K, were also increased. The expression of Cebpb, Cebpd and Ccl2 mRNAs in the aortas from fructose-fed rats were significantly elevated, by 330, 300 and 300%, respectively, compared with those of controlfed rats. The induction Ccl2 mRNA expression in the aortas was significantly correlated with the expression of Cebpb and Cebpd mRNAs in the aortas. Furthermore, the ChIP assay showed elevated binding of C/EBP-β to the 5′ upstream region of Ccl2 in the aortas from fructose-fed rats. Conclusions/interpretation These findings clearly indicate the role of C/EBPs in the mechanism of upregulation of CCL2, an inflammation-related protein, observed in the hyperinsulinaemic state, which may initiate the process of atherosclerosis.

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Inflammation as a Cardiovascular Risk Factor

Abstract: Abstract-Inflammation

Cited by 937 publications

References 98 publications

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

Comparison Between Serum hsCRP and LDL Cholesterol for Search of a Better Predictor for Ischemic Heart Disease

An immune origin of type 2 diabetes?

Increased expression of CCAAT/enhancer binding protein-β and -δ and monocyte chemoattractant protein-1 genes in aortas from hyperinsulinaemic rats

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