Norepinephrine-induced cardiac hypertrophy and fibrosis are not due to mast cell degranulation

Briest, Wilfried; Raβler, Beate; Deten, Alexander; Zimmer, Heinz‐Gerd

doi:10.1016/s0022-2828(02)91015-1

Cited by 7 publications

(7 citation statements)

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“…Furthermore, the increased expression of collagen I and III and MMP-2 by isoproterenol was suppressed by metformin. Since collagen and MMP are involved in cardiac fibrosis and are increased by catecholamine [28,29], reduced expression of these genes by metformin also support the beneficial effect of metformin in cardiac hypertrophy.…”

Section: Discussionmentioning

confidence: 85%

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Cha

Choi

Kim

et al. 2010

Korean J Physiol Pharmacol

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ABBREVIATIONS: AMPK, AMP-activated protein kinase; ANP, atrial natriuretic peptide; GPx1, glutathione peroxidase 1; IL-6, interleukin-6; MMP-2, matrix metallopeptidase 2; MMP-9, matrix metallopeptidase 9; TGF-β, transforming growth factor-β. The present study examined whether metformin treatment prevents isoporterenol-induced cardiac hypertrophy in mice. Chronic subcutaneous infusion of isoproterenol (15 mg/kg/24 h) for 1 week using an osmotic minipump induced cardiac hypertrophy measured by the heart-to-body weight ratio and left ventricular posterior wall thickness. Cardiac hypertrophy was accompanied with increased interleukin-6 (IL-6), transforming growth factor (TGF)-β, atrial natriuretic peptide (ANP), collagen I and III, and matrix metallopeptidase 2 (MMP-2). Coinfusion of metformin (150 mg/kg/24 h) with isoproterenol partially inhibited cardiac hypertrophy that was followed by reduced IL-6, TGF-β, ANP, collagen I and III, and MMP-2. Chronic subcutaneous infusion of metformin did not increase AMP-activated protein kinase (AMPK) activity in heart, although acute intraperitoneal injection of metformin (10 mg/kg) increased AMPK activity. Isoproterenol increased nitrotyrosine levels and mRNA expression of antioxidant enzyme glutathione peroxidase and metformin treatment normalized these changes. These results suggest that metformin inhibits cardiac hypertrophy through attenuating oxidative stress.

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Section: Discussionmentioning

confidence: 85%

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Cha

Choi

Kim

et al. 2010

Korean J Physiol Pharmacol

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“…Together with in vitro cell culture studies, the authors suggest a possible link between circulating norepinephrine levels and MMP-2 activation [58]. Likewise, NE infusion in rats resulted in an increase of collagen type-I, collagen type-III, MMP-2 and TIMP-2 mRNA 3 days post-infusion [59]. Whether these effects are directly related to the actions of NE, or whether other bioactive molecules are involved remains to be determined.…”

Section: Sympathetic Activationmentioning

confidence: 90%

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

Deschamps

Spinale²

2006

Cardiovascular Research

167

128

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The structural basis for the development of congestive heart failure (CHF) is a maladaptive myocardial remodeling process which occurs secondarily to post-myocardial infarction (MI), hypertensive hypertrophy, or cardiomyopathy. Both cellular and extracellular factors are involved in the remodeling process and it is the combined action of these factors giving rise to changes in myocardial structure which eventually affects function. One component in this remodeling process is a family of extracellular matrix degrading enzymes, the matrix metalloproteinases or MMPs. Many bioactive molecules such as cytokines/chemokines, bioactive peptides, and neurohormones which are operative in CHF likely contribute to the induction of MMPs. For example, a specific cassette of transcription factors is likely induced with extracellular stimuli in the context of CHF which in turn induces MMPs and contributes to the maladaptive remodeling process. This review will briefly discuss the biology of the MMP family, but will more importantly identify how biological factors active in CHF result in the modulation of the MMP family. Understanding how upstream molecules are involved in MMP regulation/dysregulation may provide an avenue to develop important therapeutic interventions.

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“…Thus increased levels of a number of signaling molecules such as ANG II and ET in the context of myocardial remodeling and heart failure are likely due, at least in part, to systemic neurohormonal activation and the elaboration of NE. NE infusion in rats resulted in an increased MMP-2 mRNA 3 days post infusion (42). In addition to the indirect effects of NE on MMP transcription, it is likely that NE can directly influence MMP transcription through activation of the ␤-and ␣-receptor pathways (79,393).…”

Section: Modification Of Mmp Transcription By Prototypical Stimulimentioning

confidence: 99%

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

Spinale¹

2007

Physiological Reviews

1,008

1,023

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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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Norepinephrine-induced cardiac hypertrophy and fibrosis are not due to mast cell degranulation

Cited by 7 publications

References 0 publications

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Metformin Inhibits Isoproterenol-induced Cardiac Hypertrophy in Mice

Pathways of matrix metalloproteinase induction in heart failure: Bioactive molecules and transcriptional regulation

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

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