Circulating matrix metalloproteinase-9 concentrations and abdominal aortic aneurysm presence: a meta-analysis

Takagi, Hisato; Manabe, Hideaki; Kawai, Norikazu; Goto, Shin-nosuke; Umemoto, Takuya

doi:10.1510/icvts.2009.208835

Cited by 66 publications

(39 citation statements)

References 13 publications

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“…Numerous molecules including MMPs, C-reactive protein (CRP) and D-Dimer have shown promise in the prediction of acute aortic dissection. 13 A recent meta-analysis implicated measurement of circulating MMP-9 as an indicator of abdominal aortic aneurysm (AAA) disease, 14 and plasma measurement of MMP-1 and MMP-9 has been shown to be predictive of aortic rupture. 15 Further, composite measurement of high density lipoprotein (HDL), CRP and immunoglobulin G correlates to AAA size.…”

Section: Discussionmentioning

confidence: 99%

Plasma biomarkers for distinguishing etiologic subtypes of thoracic aortic aneurysm disease

Ikonomidis

Ivey

Wheeler

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

105

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Background Thoracic aortic aneurysms (TAAs) develop through an asymptomatic process resulting in gross dilatation that progresses to rupture if left undetected and untreated. If detected, TAA patients are followed over time until the risk of rupture outweighs the risk of surgical repair. Current methodologies for tracking TAA size are limited to expensive computed tomography or magnetic resonance imaging, as no acceptable population screening tools are currently available. Previous studies from this laboratory and others have identified differential protein profiles for the matrix metalloproteinases (MMPs) and their endogenous tissue inhibitors (TIMPs), in ascending TAA tissue from patients with bicuspid aortic valves (BAV), versus patients with idiopathic degenerative disease and a tricuspid aortic valve (TAV). Additionally, altered microRNA (miR) expression levels have also been reported in TAAs as compared to normal aortic tissue. The objective of the present study was to identify circulating factors within the plasma that could serve as potential biomarkers for distinguishing etiological subtypes of aneurysm disease. Methods Ascending TAA tissue and plasma specimens were obtained from BAV (n=21) and TAV (n=21) patients at the time of surgical resection. The protein abundance of key MMPs (-1, -2, -3, -8, -9) and TIMPs (-1, -2, -3, -4), and microRNAs (-1, -21, -29a, -133a, -143, -145) was examined using a multi-analyte protein profiling system or by quantitative PCR, respectively. Results were compared to normal aortic tissue and plasma obtained from patients without aortic disease (n=10). Results Significant (p < 0.05) differences in standardized miR-1 and miR-21 abundance between BAV and TAV aortic tissue samples and different tissue and plasma profiles of analyte differences from normal aorta where observed between the BAV and TAV groups. Linear regression analysis significant linear relationships in plasma and tissue measurements only for MMP-8 and TIMPs -1, -3 and -4 (p < 0.05). Receiver operator curve analysis revealed specific cassettes of analytes predictive of TAA disease. Relative to normal aorta, BAV proteolytic balance was significantly increased for MMP-1, -2 and -7, and for decreased MMP-8 and -9. In contrast, TAV proteolytic balance relative to normal aorta was significantly increased only for MMP-1 and decreased for MMP-8 and -9. Conclusions Taken together these unique data demonstrate differential plasma profiles of MMPs, TIMPs, and miRs in ascending TAA specimens from patients with BAV and TAV. These results suggest that circulating biomarkers may form the foundation for a broader platform of biomarkers capable of detecting the presence of TAA using a simple blood test and may also be useful in personalized medicine strategies to distinguish between etiological subtypes of TAAs in patients with aneurysm disease.

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Section: Discussionmentioning

confidence: 99%

Plasma biomarkers for distinguishing etiologic subtypes of thoracic aortic aneurysm disease

Ikonomidis

Ivey

Wheeler

et al. 2013

The Journal of Thoracic and Cardiovascular Surgery

105

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“…The level of circulating MMP-9 was significantly higher in patients with AAA than in those without AAA. Moreover, recent study reported that the level of MMP-9 in the plasma was statistically elevated in patients with ruptured AAA, compared to patients with nonruptured AAA [19]. Strikingly, it was reported that the inhibition of MMP activity prevented the development of AAA.…”

Section: Discussionmentioning

confidence: 99%

Curcumin Attenuates Angiotensin II‐Induced Abdominal Aortic Aneurysm by Inhibition of Inflammatory Response and ERK Signaling Pathways

Hao

Wang

et al. 2014

Evidence-Based Complementary and Alternative Medicine

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Background and Objectives. Curcumin has long been used to treat age-related diseases, such as atherosclerosis and coronary heart disease. In this study, we explored the effects of curcumin on the development of abdominal aortic aneurysm (AAA). Methods. ApoE−/− mice were randomly divided into 3 groups: AngII group, AngII + curcumin (AngII + Cur) group (100 mg/kg/d), and the control group. Miniosmotic pumps were implanted subcutaneously in ApoE−/− mice to deliver AngII for 28 days. After 4-week treatment, abdominal aortas with AAA were obtained for H&E staining, immunohistochemistry, and Western blotting. Results. The results showed that curcumin treatment significantly decreased the occurrence of AAA. The levels of macrophage infiltration, monocyte chemoattractant protein-1 (MCP-1), and tumor necrosis factors-α (TNF-α) were significantly lower in AngII + Cur group than those in AngII group (all P < 0.01). The level of superoxide dismutase (SOD) was significantly higher in AngII + Cur group than those in AngII group (P < 0.01). The ERK1/2 phosphorylation in AngII + Cur group was significantly lower than that in AngII group (P < 0.01). Conclusions. These results suggested that curcumin can inhibit the AngII-induced AAA in ApoE−/− mice, whose mechanisms include the curcumin anti-inflammation, antioxidative stress, and downregulation of ERK signaling pathway.

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“…MMPs are involved in flow-induced outward vascular remodeling 122 and several aspects of cardiovascular remodeling, e.g., left ventricular hypertrophy, atherosclerosis, and/or aortic aneurysm. [123][124][125] Several studies on CKD patients showed serum-level variations of MMPs and their inhibitors. 126,127 Arterial enlargement, arterial stiffening, and increased circumferential wall stress occurred in parallel with GFR decline, but their relative importance is more complex.…”

Section: Arterial Remodeling and Stiffness In Ckd Stages 2-5mentioning

confidence: 99%

Arterial stiffness and pulse pressure in CKD and ESRD

Briet

Boutouyrie

Laurent

et al. 2012

Kidney International

326

238

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We recognize that increased systolic pressure is the most challenging form of hypertension today and that pulse pressure as an independent cardiovascular risk factor has focused attention on arterial stiffness and wave reflections as the most important factors determining these pressures. In recent years, many studies emphasized the role of arterial rigidity in the development of cardiovascular diseases, and it was shown that stiffening of arteries is associated with increased cardiovascular mortality and morbidity. Moreover,arterial stiffening is linked to decreased glomerular filtration rate, and is predictive of kidney disease progression and the patient’s cardiovascular outcome. Premature vascular aging and arterial stiffening are observed with progression of chronic kidney disease (CKD) and in end-stage renal disease(ESRD). This accelerated aging is associated with outward remodeling of large vessels, characterized by increased arterial radius not totally compensated for by artery wall hypertrophy. Arterial stiffening in CKD and ESRD patients is of multifactorial origin with extensive arterial calcifications representing a major covariate. With aging, the rigidity is more pronounced in the aorta than in peripheral conduit arteries, leading to the disappearance or inversion of the arterial stiffness gradient and less protection of the microcirculation from high-pressure transmission. Various non-pharmacological or pharmacological interventions can modestly slow the progression of arterial stiffness,but arterial stiffness is, in part, pressure dependent and treatments able to stop the process mainly include antihypertensive drugs.

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Circulating matrix metalloproteinase-9 concentrations and abdominal aortic aneurysm presence: a meta-analysis

Cited by 66 publications

References 13 publications

Plasma biomarkers for distinguishing etiologic subtypes of thoracic aortic aneurysm disease

Plasma biomarkers for distinguishing etiologic subtypes of thoracic aortic aneurysm disease

Curcumin Attenuates Angiotensin II‐Induced Abdominal Aortic Aneurysm by Inhibition of Inflammatory Response and ERK Signaling Pathways

Arterial stiffness and pulse pressure in CKD and ESRD

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