Collagen type-I degradation is related to arterial stiffness in hypertensive and normotensive subjects

McNulty, Marie; Mahmud, Azra; Spiers, Paul; Feely, J.

doi:10.1038/sj.jhh.1002015

Cited by 88 publications

(79 citation statements)

References 33 publications

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“…53 Other authors have reported an inverse association between arterial stiffness and plasma MMP-1 in hypertensive patients. 54 Although no cardiac parameters were included in a multiple regression analysis to assess whether they influenced the correlations between arterial stiffness and serum biomarkers, these observations suggest that in arterial hypertension, alterations in these molecules may reflect disturbances of collagen metabolism that occur not just at the myocardial but also at the arterial wall level.…”

Section: Aspects Related To the Presence Of Comorbiditiesmentioning

confidence: 99%

Circulating Biomarkers of Collagen Metabolism in Cardiac Diseases

2010

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A lterations of the structure and composition of cardiomyocyte and noncardiomyocyte compartments of the myocardium appear to play a central role in the pathogenesis of heart failure (HF) associated with a number of cardiac diseases. Among these alterations, changes in the quantity and quality of the extracellular matrix, including the collagen network, have been characterized that induce remodeling of the myocardium and ultimately deteriorate left ventricular (LV) function and facilitate the development of HF. Studies on circulating biomarkers of collagen metabolism have attracted the attention of the medical community, and some circulating biomarkers have been proposed as potential useful tools to improve diagnosis, prognosis, and therapy in cardiac diseases that develop HF. 1 However, the available data are far from conclusive and from affording incremental value to the knowledge provided by more classic diagnostic tools. This is due mainly to 3 limitations. First, collagen is the most abundant protein in the body, and its turnover is so dynamic that not all circulating molecules proposed as biomarkers actually reflect changes in collagen metabolism, namely at the cardiac level. Second, a thorough understanding of the association of a given biomarker with the pathological features of the collagen network in the cardiac disease under study has not been considered essential, thus weakening its pathophysiological meaning. Third, several methodological issues may introduce a number of confounding factors into the measurements of circulating biomarkers of collagen metabolism, thus bringing into question the validity of the available results. Therefore, this article is not aimed at providing a systematic review of all the published information on circulating biomarkers of collagen metabolism in cardiac diseases but at analyzing the biochemical, pathophysiological, and methodological aspects to be taken into account to overcome the above limitations and to improve the clinical applicability of such molecules. Circulating Biomarkers of Collagen Metabolism Collagen MetabolismThe extracellular matrix contains a fibrillar collagen network, a basement membrane, proteoglycans and glycosaminoglycans, and bioactive signaling molecules. The collagen network is a metabolically active structure in the sense that the balance between the synthesis and degradation of collagen determines its turnover, which is estimated to be from 80 to 120 days. 2 The turnover is regulated by fibroblasts and by fibroblasts differentiated to myofibroblasts (Figure 1). 3 These cells respond to mechanical stretch, autocrine and paracrine factors generated locally (eg, vasoactive peptides such as angiotensin II and growth factors such as transforming growth factor-␤ or connective tissue growth factor), and hormones derived from the circulation (eg, aldosterone). In addition, a number of proinflammatory cytokines (eg, tumor necrosis factor-␣, interleukin-1 and -6) secreted by monocytes and macrophages also influence the function of fibroblasts and my...

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Section: Aspects Related To the Presence Of Comorbiditiesmentioning

confidence: 99%

Circulating Biomarkers of Collagen Metabolism in Cardiac Diseases

2010

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“…19 We have shown previously a strong association between aortic stiffness and collagen turnover in hypertensive patients. 20 After the initial degradation by collagenases (MMP-1, MMP-8, MMP-13) and elastinase (MMP-7), further degradation of ECM basement membrane takes place by activation of MMP-9. 8 The MMP-9 À1562C4T polymorphism is a promoter polymorphism and the T-allele enhances the expression of the MMP-9 messenger RNA in cells.…”

Section: Mmp-9 Gene and Arterial Stiffness In Hypertension S Zhou Et Almentioning

confidence: 99%

Matrix metalloproteinase-9 polymorphism contributes to blood pressure and arterial stiffness in essential hypertension

et al. 2007

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Arterial stiffness is an independent predictor of cardiovascular events in a hypertensive population. Serum levels of matrix metalloproteinase (MMP)-9 are associated with arterial stiffness and predict cardiovascular risk. We investigated the role of MMP-9 polymorphism À1562C4T on blood pressure (BP) and arterial stiffness in a newly diagnosed hypertensive population. Untreated hypertensive patients (n ¼ 215, mean age 46713 years) were studied. Supine BP, carotid-femoral pulse wave velocity (PWV) and augmentation index were assessed. Serum biochemistry and plasma MMP-9 concentrations were measured and genotyping performed following extraction of genomic DNA. BP, aortic PWV and serum MMP-9 levels were significantly higher in T-allele carriers of the À1562C4T polymorphism with a significant gene-dose effect (Po0.0001). In a stepwise regression model adjusting for known or likely determinants, the 1562C4T polymorphism emerged as an independent predictor of systolic BP (R 2 ¼ 0.25, Po0.0001), diastolic BP (R 2 ¼ 0.16, Po0.0001) and PWV (R 2 ¼ 0.47,Po0.0001). This is the first study to show the effect of MMP-9 polymorphism on BP and aortic stiffness in a hypertensive population. These results suggest that hypertensive patients carrying the T allele may be at increased risk of cardiovascular events.

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“…Associations between collagen synthesis and degradation and arterial stiffness have been demonstrated in normotensive and hypertensive individuals (McNulty et al 2006) , and patients with dilated cardiomyopathy (Bonapace et al 2006). However, this is a relatively new area of research, and further work is needed to delineate the relationship between collagen turnover and arterial stiffness.…”

Section: Arterial Stiffnessmentioning

confidence: 99%

Effects of acute and chronic low-volume high-intensity interval exercise on cardiovascular health in patients with coronary artery disease

Currie

2013

Appl. Physiol. Nutr. Metab.

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The merits of low-volume high-intensity interval exercise (HIT) have been established in healthy populations; however, no studies have examined this exercise prescription in patients with coronary artery disease (CAD). The present thesis examined the acute and chronic effects of HIT in patients with CAD. The first study demonstrated transient improvements in brachial artery endothelial-dependent function, which was assessed using flow-mediated dilation (FMD) 60 min following a single bout of either HIT or moderate-intensity endurance exercise (END) in habitually active patients. The second study demonstrated no effects of training status on the acute endothelial responses to exercise; following 12-weeks of either HIT or END training. However, there was a significant reduction in endothelial-independent function immediately postexercise, at both pre- and post-training, which requires further examination. The third study demonstrated comparable increases in fitness and resting FMD following 12-weeks of END and HIT, lending support to the notion that favourable adaptations are obtainable with a smaller volume of exercise. Finally, the fourth study demonstrated no change in heart rate recovery following 12-weeks of END and HIT. However, pre-training heart rate recovery values reported by our sample were in a low risk range, which suggests training induced improvements may only be achievable in populations with attenuated pre-training values. The results of this thesis provide preliminary evidence that supports the use of HIT in patients with CAD. The findings of favourable transient and chronic improvements following HIT are notable, especially given that the HIT protocol involves less time and work than END, which was modelled after the current exercise prescription in cardiac rehabilitation. Further investigations are necessary, including the assessment of additional physiological indices; the feasibility and adherence to HIT; the inclusion of CAD populations with comorbidities, including heart failure and diabetes; as well as other forms of HIT training, including HIT combined with resistance training.

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Collagen type-I degradation is related to arterial stiffness in hypertensive and normotensive subjects

Cited by 88 publications

References 33 publications

Circulating Biomarkers of Collagen Metabolism in Cardiac Diseases

Circulating Biomarkers of Collagen Metabolism in Cardiac Diseases

Matrix metalloproteinase-9 polymorphism contributes to blood pressure and arterial stiffness in essential hypertension

Effects of acute and chronic low-volume high-intensity interval exercise on cardiovascular health in patients with coronary artery disease

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