C-reactive protein (CRP): more than just an innocent bystander?

Paraskevas, Kosmas I.; Mikhailidis, Dimitri P.

doi:10.1185/030079908x253654

Cited by 40 publications

(25 citation statements)

References 63 publications

(29 reference statements)

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“…Whether CRP really is an independent risk factor for CVD remains debatable [19], however studies have shown that even small differences in CRP concentrations can reflect the risk of developing CVD [20]. In the present study, 12% of those examined at baseline did not come to the 3-month examination and 21% did not come to the 1-year follow-up.…”

Section: Discussioncontrasting

confidence: 51%

Periodontal treatment influences risk markers for atherosclerosis in patients with severe periodontitis

et al. 2009

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a b s t r a c tThis study investigated the effect of mechanical infection control for periodontitis and periodontal surgery on the prevalence of well-established risk factors for atherosclerosis, and plasma levels of cytokines, antibodies against heat shock proteins and markers of systemic inflammation.Sixty-eight patients between 39 and 73 years of age with severe periodontitis who had been referred to four specialist periodontology clinics in Sweden were investigated. A fasting venous blood sample was taken at baseline and additional samples were collected after 3 and 12 months. A total of 54 patients underwent periodontal treatment.The periodontal treatment was successful, as pathogenic gingival pockets decreased significantly. Plasma glucose, lipids and markers of systemic inflammation were not significantly altered after 3 months. One year after the initial treatment, HDL-C concentrations were significantly increased ( 0.08 mmol/L) whereas LDL-C concentrations decreased ( 0.23 mmol/L). Haptoglobin concentrations were also lower. Interleukin-18 and interferon-␥ levels were also lower after 12 months (60 ng/L (−23%) and 11 ng/L (−97%) respectively). Treatment had no effect on plasma levels of IgA, IgG1, IgG2 antibodies against heat shock proteins.In conclusion, this study indicates that standard treatment for periodontal disease induces systemic changes in several biochemical markers that reflect the risk for atherosclerosis.

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Section: Discussioncontrasting

confidence: 51%

Periodontal treatment influences risk markers for atherosclerosis in patients with severe periodontitis

et al. 2009

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“…25 In addition, smoking adversely influences several emerging risk factors (eg, C-reactive protein and fibrinogen). 9,12,54,55 Family history may also have an effect on the development of a specific vascular disease. For example, type I 56,57 and especially type II 58,59 DM are partly inherited disorders.…”

Section: Discussionmentioning

confidence: 99%

“…[1][2][3][4][5][6] There is also accumulating evidence supporting the role of several emerging risk factors (such as creatinine, fibrinogen, and C-reactive protein). [6][7][8][9] Modification of these risk factors may play a role in the pathogenesis of vascular disease. For example, smoking cessation is associated with reduced arterial stiffness 10 ; heavy alcohol consumption is associated with an increase in the prevalence of the metabolic syndrome, diabetes mellitus (DM), peripheral arterial disease (PAD), stroke, coronary heart disease (CHD), and overall cardiovascular disease.…”

Section: Smokingmentioning

confidence: 99%

Do Different Vascular Risk Factors Affect All Arteries Equally?

et al. 2008

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“…Vascular inflammation, a key mediator of which is CRP, 33 is increasingly recognized to be associated with a number of cardiovascular diseases, including atherosclerosis 34 and peripheral vascular disease. 13 In female offspring, CRP was elevated in the PR group and restored to control levels by administration of atorvastatin, in a manner that mirrored the effects on MA endothelial function.…”

Section: Discussionmentioning

confidence: 99%

Atorvastatin Restores Endothelial Function in Offspring of Protein-Restricted Rats in a Cholesterol-Independent Manner

et al. 2009

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Abstract-Maternal protein restriction in rats leads to endothelial dysfunction and decreased NO bioavailability in the offspring. Statins (3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors) are recognized to have pleiotropic actions including increasing NO bioavailability and reducing inflammation and oxidative damage. This study assessed statin treatment on vascular function in a model of endothelial dysfunction, which is independent of dyslipidemia. Wistar rats were fed a control (18% casein) or protein-restricted (9% casein) diet throughout pregnancy. At weaning, a subset of the protein-restricted group was given atorvastatin (10 mg/kg per day) in the drinking water. At 145 days of age, offspring were euthanized by CO 2 inhalation. Plasma samples were collected for markers of inflammation, vascular reactivity of the thoracic aorta, and small mesenteric arteries were assessed on the wire myograph, and tissues were snap frozen for molecular biology analysis. Thoracic aorta endothelial-dependent vasodilatation was attenuated in the male offspring from both protein-restricted groups compared with controls (PϽ0.05) but was similar in females (P value not significant). Endothelial-dependent dilatation of mesenteric arteries was attenuated in male and female protein-restricted offspring (PϽ0.05) and was corrected by atorvastatin. Maternal protein restriction increased plasma inflammatory markers granulocyte chemotactic protein, lipocalin-2, and ␤ 2 -microglobulin in male and C-reactive protein in female offspring (PϽ0.05). Atorvastatin had no effect on inflammatory markers in the males but restored C-reactive protein to control levels in the females (PϽ0.05). Aortic and mesenteric artery mRNA levels of endothelial NO synthase, superoxide dismutase 1, and tumor necrosis factor-␣ were unchanged. These data suggest that atorvastatin can restore endothelial function in this model, but its effects are gender specific and dependent on the vascular bed. Key Words: statins (atorvastatin) Ⅲ experimental models Ⅲ fetal programming Ⅲ vascular biology Ⅲ endothelium Ⅲ nitric oxide Ⅲ inflammation T here is considerable evidence that the etiology of cardiovascular and metabolic diseases has origins partly in the developmental environment. 1 A widely used animal model to study this phenomenon is the rat, in which the restriction of dietary protein during pregnancy leads to raised blood pressure and endothelial dysfunction in the offspring. [2][3][4] Increasingly, evidence from this model points to a disruption to the NO pathway as a key component of the underlying pathophysiology. 4,5 The healthy vascular endothelium plays an important role in maintaining vascular tone through the release of factors including NO, prostacyclin, and endothelial-derived hyperpolarizing factor. 6 The importance of a healthy endothelium is seen in cardiovascular and metabolic diseases, where endothelial dysfunction is associated with atherosclerosis, hypertension, and the metabolic syndrome. 7-9 Important in the development of such endothelial ...

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C-reactive protein (CRP): more than just an innocent bystander?

Cited by 40 publications

References 63 publications

Periodontal treatment influences risk markers for atherosclerosis in patients with severe periodontitis

Periodontal treatment influences risk markers for atherosclerosis in patients with severe periodontitis

Do Different Vascular Risk Factors Affect All Arteries Equally?

Atorvastatin Restores Endothelial Function in Offspring of Protein-Restricted Rats in a Cholesterol-Independent Manner

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