Selective Induction of Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases in Atrial and Ventricular Myocardium in Patients With Atrial Fibrillation

Mukherjee, Rupak; Herron, Amanda R.; Lowry, Abigail S.; Stroud, Robert E.; Stroud, Martha R.; Wharton, J. Marcus; Ikonomidis, John S.; Crumbley, Arthur J.; Spinale, Francis G.; Gold, Michael R.

doi:10.1016/j.amjcard.2005.08.073

Cited by 85 publications

(66 citation statements)

References 27 publications

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“…While it remains to be established, it is likely that these differences in chamber specific MMP profiles are due to a combination of factors that include inherent differences in loading conditions, embryological origin, and cellular response to biological stimuli. With respect to TIMPs, all four TIMPs have been identified within the normal human myocardium (15,158,206,230,285,406,444). A robust signal for the cardiovascular-specific TIMP, TIMP-4, has been demonstrated in all four chambers of the human heart (229,285,444).…”

Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 91%

“…With respect to TIMPs, all four TIMPs have been identified within the normal human myocardium (15,158,206,230,285,406,444). A robust signal for the cardiovascular-specific TIMP, TIMP-4, has been demonstrated in all four chambers of the human heart (229,285,444). Thus a full complement of MMPs and TIMPs exists within the normal adult human myocardium, and therefore, changes in the abundance and relative ratios of these proteolytic enzymes and inhibitors would likely contribute to changes in the myocardial matrix, which in turn would affect overall geometry and function.…”

Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 99%

“…thereby provided evidence that a localized proteolytic pathway existed for pro-MMP activation (406,444). With the use of an immunohistochemical approach as well as a quantitative immunochemical approach, it has been demonstrated that MMP distribution may be chamber specific (158,206,285). For example, the relative levels of certain MMPs, such as MMP-1, appear lower in the right ventricle compared with the left ventricle (158,206).…”

Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 99%

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Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

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It is now becoming apparent that dynamic changes occur within the interstitium that directly contribute to adverse myocardial remodeling following myocardial infarction (MI), with hypertensive heart disease and with intrinsic myocardial disease such as cardiomyopathy. Furthermore, a family of matrix proteases, the matrix metalloproteinases (MMPs) and the tissue inhibitors of MMPs (TIMPs), has been recognized to play an important role in matrix remodeling in these cardiac disease states. The purpose of this review is fivefold: 1) to examine and redefine the myocardial matrix as a critical and dynamic entity with respect to the remodeling process encountered with MI, hypertension, or cardiomyopathic disease; 2) present the remarkable progress that has been made with respect to MMP/TIMP biology and how it relates to myocardial matrix remodeling; 3) to evaluate critical translational/clinical studies that have provided a cause-effect relationship between alterations in MMP/TIMP regulation and myocardial matrix remodeling; 4) to provide a critical review and analysis of current diagnostic, prognostic, and pharmacological approaches that utilized our basic understanding of MMP/TIMPs in the context of cardiac disease; and 5) most importantly, to dispel the historical belief that the myocardial matrix is a passive structure and supplant this belief that the regulation of matrix protease pathways such as the MMPs and TIMPs will likely yield a new avenue of diagnostic and therapeutic strategies for myocardial remodeling and the progression to heart failure.

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Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 91%

Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 99%

Section: A Mmp Expression In Normal Adult Myocardiummentioning

confidence: 99%

See 1 more Smart Citation

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Spinale¹

2007

Physiological Reviews

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“…In addition, when AGEs interact with AGE receptors (RAGE), the production of matrix metalloproteinases (MMPs) and tissue growth factor-beta were stimulated. [37][38][39] All of these actions together lead to atrial fibrosis, resulting in multiple wavelets and reentrant anchor points in atria. A recent clinical study also found that the serum AGE level was higher in AF patients with or without diabetes mellitus.…”

Section: Discussionmentioning

confidence: 99%

Beneficial Effects of Pioglitazone on Retardation of Persistent Atrial Fibrillation Progression in Diabetes Mellitus Patients

Liu

Wang

2014

Int. Heart J.

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SummaryThis study aimed to explore the effects of pioglitazone treatment on progression from persistent atrial fibrillation (AF) to permanent atrial fibrillation in diabetes mellitus (DM) patients and to investigate the possible mechanisms involved in those effects.A total of 146 diabetes mellitus (DM) patients with firstly identified persistent AF were selected. Seventy patients were randomized into the pioglitazone (30 mg/day) group and 76 into the placebo group. Pro-collagen type I carboxyterminal peptide (PICP), advanced glycation end products (AGEs), and angiotensin II were assayed and left atrial diameter (LA diameter) was measured at the first presence of persistent AF, and at 6 and 14 months of follow-up. The time point of identification of permanent AF and the incidence of permanent AF in the patients were all recorded.Thirty-seven (49%) of the 76 patients in the placebo group and 21 (30%) of the 70 patients in the pioglitazone group progressed to permanent AF (P = 0.028). No significant differences existed in the follow-up time (20.5 ± 3.97 months for pioglitazone group versus 20.9 ± 4.14 months for placebo group) between the two groups (P = 0.535). In the pioglitazone group, no significant change was found in angiotensin II level. The PICP level did not change significantly at 6-months of follow-up, but decreased significantly at 14-months of follow-up (P = 0.032). The AGE (P = 0.037 at 6-month follow-up, P < 0.035 at 14-month follow-up) level was significantly lower at both 6 and 14-months of followup.By lowering the PICP level, pioglitazone treatment may decrease the incidence of permanent AF in DM patients with persistent AF, which may be associated with the suppressing effect of pioglitazone on AGEs. (Int Heart J 2014; 55: 499-505)

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“…These products of degradation serve as a stimulus to collagen synthesis, thus increasing the deposition of poorly structured fibrotic tissue. These enzymes Review have been used recently in atrial remodeling in congestive heart failure [Mukherjee et al 2006] and also in patients with AF [Gramley et al 2007].…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Review: Atrial fibrillation and renin-angiotensin system

Serra

Boccadoro

2008

Therapeutic Advances in Cardiovascular Disease

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Atrial Fibrillation (AF) is one of the most frequent arrhythmias, especially in elderly patients. Cardiac overload increases the incidence of AF. Clinical presentation of atrial fibrillation can occur as nonsustained paroxysms, persistent episodes and in chronic-permanent form. The physio-pathological mechanisms are:• Circuit of multiple and anarchic re-entries • Atrial fibrillatory conduction • Re-entry circuit with fibrillatory conduction. Remodeling (electrical or structural) facilitates the appearance and persistence of AF: Neurovegetative changes and cytosolic Ca overload facilitate AF. Interstitial atrial fibrosis, in which Renin-Angiotensin System (RAS) hyperactivity is a main aspect of remodeling. There is clinical evidence that supports the antiatrial fibrillatory actions of RAS blockade. Potential mechanisms are: (a) direct modulation of ionic channels, (b) hemodynamic improvement, (c) reduction of atrial stretching, (d) antifibrotic effects. There is less clinical evidence with antialdosterone drugs, but theoretically these might also be useful. Keywords: atrial fibrillation, remodeling, renin-angiotensin systemAtrial fibrillation, pathophysiology, remodeling. Atrial fibrillation (AF) is one of the most frequent arrhythmias in adulthood, with its incidence increasing with age. The situations and pathologies that lead to hemodynamic or pressure overload are associated to AF. This can be present as nonsustained paroxysms, persistent episodes (reverted to Sinus Rhythm by medical treatments) and as chronic-permanent AF. It is referred to as 'isolated' when there is no structural cardiopathy or other morbid entities that can explain it. Three mechanisms have been described to explain its physiopathogenia [Nattel and Ehrlich, 2004]: a. Multiple, coexistent, anarchic re-entry circuits. AF settles down if the conditions are appropriate for them to appear and persist over time. These alterations involve refractoriness (reduction), velocity of conduction (delay), and an increase in heterogeneity of both properties [Moe and Abildskov, 1995;Cosio, 1994;Cosio and Arribas, 1989;Allessie, et al. 1985;Moe, 1962]. The quantity of atrial 'mass' (atrial volume) is also a determining factor. For hearts with big atria, AF is more frequent and lasting [Henry et al. 1976]. The persistence of the fibrillatory state depends on the number of the aforementioned re-entries circuits that are simultaneously present, at any determined moment. Few coexistent re-entries diminish the possibility of persistence.b. Rapid and continued ectopic activity, with 'fibrillatory conduction' in auricles, due to its impossibility to respond in an organized form.c. Only one circuit of re-entry with 'fibrillatory conduction,' with this 'fibrillatory conduction' also depending on the heterogeneity of refractoriness and atrial conductivity.An interrelationship may exist between these three mechanisms.An episode of AF needs a 'trigger' (premature beats, tachycardia) to initiate it, by interaction with 'modulators' (neurovegetative system, br...

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Selective Induction of Matrix Metalloproteinases and Tissue Inhibitor of Metalloproteinases in Atrial and Ventricular Myocardium in Patients With Atrial Fibrillation

Cited by 85 publications

References 27 publications

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Myocardial Matrix Remodeling and the Matrix Metalloproteinases: Influence on Cardiac Form and Function

Beneficial Effects of Pioglitazone on Retardation of Persistent Atrial Fibrillation Progression in Diabetes Mellitus Patients

Review: Atrial fibrillation and renin-angiotensin system

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