Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacing-induced atrial fibrillation

Chen, Chien Lung; Huang, Shoei K. Stephen; Lin, Jiunn Lee; Lai, Ling; Lai, Shao Chuan; Liu, Chia Wei; Chen, Wen Chi; Wen, Cheng; Lin, Chih Sheng

doi:10.1016/j.yjmcc.2008.07.007

Cited by 69 publications

(50 citation statements)

References 47 publications

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“…Patients with AAs showed significantly higher MMP expression levels in their aortic tissue than patients without AAs [27, 28]. Elevated MMP-2, longer AF duration, and atrial extracellular matrix remodeling of AF further increased the risk of difficulties in restoring sinus rhythm in AF patients [29-31]. Active myocardial remodeling is accompanied by enhanced activation of MMP-2 and MMP-9 [32, 33].…”

Section: Discussionmentioning

confidence: 99%

Association between Atrial Fibrillation and Aortic Aneurysms: A Population-Based Cohort Study

et al. 2018

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Objective: Atrial fibrillation (AF) is the most common form of sustained arrhythmia. Several molecular pathways associated with the pathogenesis of AF also participate in the initiation and progression of aortic aneurysm (AA). In this study, we aimed to evaluate potential associations between AA and AF. Patients and Methods: The data for this nationwide population-based retrospective cohort study were obtained from Taiwan’s National Health Insurance Research Database (NHIRD). All medical conditions for each case and the controls were categorized using the 9th revision of the International Classification of Diseases (ICD-9). Odds ratios and 95% confidence intervals for associations between AF and AA were estimated using Cox regression and adjusted for comorbidities. Results: Our analyses included 116,225 AF cases and 116,225 propensity score-matched controls. Compared with the controls, the patients with AF exhibited a significantly increased risk of developing an AA (adjusted hazard ratio, HR 1.243, p < 0.001). Another cohort of 19,776 patients diagnosed with AA were identified, and 19,776 propensity score-matched patients were included as controls. Patients who had AA were also at an increased risk of developing AF (adjusted HR 1.187, p < 0.001). Heart failure (HF) was a common risk factor for both AA and AF. Conclusion: There are associations between AF and AA. HF is a mutual risk factor for the development of AF and AA.

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Section: Discussionmentioning

confidence: 99%

Association between Atrial Fibrillation and Aortic Aneurysms: A Population-Based Cohort Study

et al. 2018

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“…In particular, many reports have demonstrated that MMP-9 plays a critical role in AF-induced myocardial matrix remodelling and could be a target for the prevention or treatment of AF (Nakano et al, 2004;Chen et al, 2008). MMP-9 is mainly responsible for degrading structural or fibrillar collagens, gelatin, elastin as well as fibronectin.…”

Section: Effects Of Spironolactone On Atrial Fibrosis and Dilatationmentioning

confidence: 99%

Effects of spironolactone on atrial structural remodelling in a canine model of atrial fibrillation produced by prolonged atrial pacing

Zhao

et al. 2010

British J Pharmacology

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Background and purpose: Suppression of the renin-angiotensin-aldosterone system can prevent atrial fibrillation (AF) by attenuating atrial structural remodelling but the role of aldosterone in AF prevention has not been investigated thoroughly. We explored whether the aldosterone antagonist, spironolactone, could improve atrial structural remodelling in long-term rapid pacing-induced AF. Experimental approach: Three groups of dogs were used, sham-operated, control and spironolactone-treated groups. Dogs in the control and spironolactone groups had right atrial pacing for 6 weeks. The spironolactone group was given spironolactone 1 week before and during the atrial pacing. After 6 weeks of pacing, atrial structural and functional changes were assessed by echocardiography, haemodynamic parameters by cardiac catheterization, histopathological changes by light and electron microscopy and cardiomyocyte apoptosis by TUNEL. Caspase-3, Bcl-2, bax, calpain I, calpastatin, matrix metalloproteinase (MMP)-9 and tissue inhibitors of metalloproteinase (TIMP)-1 were analysed by immunohistochemistry and Western blotting. The inducibility and duration of AF were measured by atrial burst pacing. Key results: After atrial pacing, the proportion of TUNEL positive cells, myolysis, atrial fibrosis and dilatation were all significantly increased and these changes were inhibited by spironolactone. Spironolactone treatment reversed the increased expression of caspase-3, bax, calpain I and MMP-9 and the decreased level of Bcl-2, calpastatin and TIMP-1, induced by chronic atrial pacing. Also spironolactone prevented the increased inducibility and duration of AF, induced by tachypacing. Conclusions and implications: Treatment with spironolactone prevented myocardial apoptosis, myolysis, atrial fibrosis and dilatation, suggesting a possible beneficial effect of aldosterone antagonism on atrial structural remodelling in AF.

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“…Increased MMP expression and activity have been reported in several animal models of ventricular dysfunction development [10]. Although increased MMP activity contributes to several cardiovascular diseases [11], including end-stage dilated cardiomyopathy and MI [12,13,14,15,16], the link between MMP activation and myocardial remodeling has not been directly examined in nonischemic heart failure induced by valvular heart disease. Recently, we reported that an infarcted myocardium and the corresponding hypertrophic heart tissue are associated with an imbalance between MMPs and TIMP-1 expression and a loss of fibronectin (FN) in rats [17].…”

Section: Introductionmentioning

confidence: 99%

Imbalance of Matrix Metalloproteinases/Tissue Inhibitor of Metalloproteinase-1 and Loss of Fibronectin Expression in Patients with Congestive Heart Failure

Yang

Ma²,

Tan³

et al. 2010

Cardiology

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Objective: Previous studies have demonstrated that an imbalance of matrix metalloproteinases (MMPs)/tissue inhibitors of metalloproteinase-1 (TIMP-1) and a loss of fibronectin are associated with postmyocardial infarction remodeling in rats. The present study was designed to examine this issue in patients with congestive heart failure (CHF). Methods: We measured plasma levels and the cardiac protein expression of MMPs/TIMP-1 and fibronectin in 39 patients with CHF and 38 controls. Results: Plasma levels of MMP-2, MMP-3, and MMP-9 tended to be higher in patients with CHF (NYHA II: 276 ± 18, 613 ± 118, and 245 ± 43 µg/l, respectively; NYHA III: 302 ± 20, 850 ± 132, and 310 ± 39 µg/l, respectively; NYHA IV: 367 ± 15, 998 ± 99, and 392 ± 27 µg/l, respectively) than in controls (213 ± 23, 485 ± 102, and 158 ± 31 µg/l, respectively), while the plasma TIMP-1 level tended to be lower in patients with CHF (NYHA II: 126 ± 12 µg/l, NYHA III: 83 ± 11 µg/l, and NYHA IV: 61 ± 12 µg/l) than in controls (208 ± 15 µg/l). Interestingly, the changes in protein expression of MMPs/TIMP-1 were consistent with their plasma concentration. Furthermore, the fibronectin level in the patients with CHF was significantly lower than in the controls. Conclusions: These data suggest that human CHF is associated with an imbalance of MMPs/TIMP-1 and a concurrent loss of fibronectin.

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Upregulation of matrix metalloproteinase-9 and tissue inhibitors of metalloproteinases in rapid atrial pacing-induced atrial fibrillation

Cited by 69 publications

References 47 publications

Association between Atrial Fibrillation and Aortic Aneurysms: A Population-Based Cohort Study

Association between Atrial Fibrillation and Aortic Aneurysms: A Population-Based Cohort Study

Effects of spironolactone on atrial structural remodelling in a canine model of atrial fibrillation produced by prolonged atrial pacing

Imbalance of Matrix Metalloproteinases/Tissue Inhibitor of Metalloproteinase-1 and Loss of Fibronectin Expression in Patients with Congestive Heart Failure

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