Carvedilol Inhibits Matrix Metalloproteinase-2 Activation in Experimental Autoimmune Myocarditis: Possibilities of Cardioprotective Application

Skrzypiec-Spring, Monika; Haczkiewicz, Katarzyna; Sapa, Agnieszka; Piasecki, Tomasz; Kwiatkowska, J; Ceremuga, Ireneusz; Woźniak, Mieczysław; Biczysko, W; Kobierzycki, Christopher; Dzięgiel, Piotr; Podhorska-Okołów, Marzena; Szeląg, Adam

doi:10.1177/1074248417725058

Cited by 14 publications

(14 citation statements)

References 33 publications

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“…Guttierez et al showed increased enzymatic activity for MMP-2 and MMP-9 in heart tissue during the acute phase of experimental Trypanosoma cruzi infection and significant decrease of heart inflammation, delayed peak in parasitemia, and improved survival rates as a result of inhibition of MMPs activity (19). In our previous study, we also showed that experimental autoimmune myocarditis in rats proceeded with an enhanced activation of MMPs in heart tissue and that inhibition of MMP-2 activity by carvedilol resulted in the reduction of troponin and myofilaments degradation and subsequent prevention of dysfunction of the mechanical function of the heart [16].…”

Section: Discussionmentioning

confidence: 85%

“…Other interesting and promising treatment options may be strategies of preventing oxidative stress-related destruction of contractile proteins [16,18]. Oxidative stress related to acute ischemia-reperfusion injury of the heart muscle leads to intracellular activation of MMPs and subsequent degradation of troponin I, myosin light chain-1, α-actinin, and titin [15].…”

Section: Discussionmentioning

confidence: 99%

“…Enhanced activation of MMPs in heart tissue was observed also in experimental autoimmune myocarditis (EAM) [16][17][18][19]. It was proved that inhibition of MMPs activity by clarithromycin and carvedilol prevented impairment of cardiac contractility in EAM rats [16,18]. Moreover, it was shown that the inhibition of MMPs in EAM by carvedilol contributed to reduced degradation of troponin I and myofilaments [16].…”

Section: Introductionmentioning

confidence: 98%

“…In the settings of oxidative stress related to acute ischemia-reperfusion MMPs undergo activation and are responsible for cleaving troponin I, myosin light chain-1, αactinin, and titin [15]. Enhanced activation of MMPs in heart tissue was observed also in experimental autoimmune myocarditis (EAM) [16][17][18][19]. It was proved that inhibition of MMPs activity by clarithromycin and carvedilol prevented impairment of cardiac contractility in EAM rats [16,18].…”

Section: Introductionmentioning

confidence: 99%

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HMG-CoA Reductase Inhibitor, Simvastatin Is Effective in Decreasing Degree of Myocarditis by Inhibiting Metalloproteinases Activation

et al. 2021

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Background: Acute myocarditis often progresses to heart failure because there is no effective, etiology-targeted therapy of this disease. Simvastatin has been shown to be cardioprotective by decreasing matrix metalloproteinases’ (MMPs) activity. The study was designed to determine whether simvastatin inhibits MMPs activity, decreases the severity of inflammation and contractile dysfunction of the heart in experimental autoimmune myocarditis (EAM). Methods: Simvastatin (3 or 30 mg/kg/day) was given to experimental rats with EAM by gastric gavage for 21 days. Then transthoracic echocardiography was performed, MMPs activity and troponin I level were determined and tissue samples were assessed under a light and transmission electron microscope. Results: Hearts treated with simvastatin did not show left ventricular enlargement. As a result of EAM, there was an enhanced activation of MMP-9, which was significantly reduced in the high-dose simvastatin group compared to the low-dose group. It was accompanied by prevention of myofilaments degradation and reduction of severity of inflammation. Conclusions: The cardioprotective effects of simvastatin in the acute phase of EAM are, at least in part, due to its ability to decrease MMP-9 activity and subsequent decline in myofilaments degradation and suppression of inflammation. These effects were achieved in doses equivalent to therapeutic doses in humans.

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Section: Discussionmentioning

confidence: 85%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

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HMG-CoA Reductase Inhibitor, Simvastatin Is Effective in Decreasing Degree of Myocarditis by Inhibiting Metalloproteinases Activation

et al. 2021

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“…At this moment, there is no effective standardized therapy for acute myocarditis, besides the optimal care of heart failure and arrhythmias in accordance with evidence-based guidelines and specific etiology-driven therapy [7,8].…”

Section: Discussionmentioning

confidence: 99%

Management of a rare case of adrenergic myocarditis complicated with cardiogenic shock

Macovei

Magopet²,

Anghel

et al. 2019

int arch med

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A 41-year-old female was referred to our clinic with progressive dyspnea and a syncope, preceded by angina. On admission she was in cardiogenic shock. ECG showed diffuse repolarization changes and cardiac enzymes were elevated. The echocardiogram revealed severe left ventricular dysfunction with basal and medium walls hypokinesia. After stabilizing the patient, a coronary angiography was performed which revealed normal epicardial arteries. In the next days her clinical status was marked by severe hypertensive episodes with flash pulmonary edema and low responsiveness to therapy. Cardiovascular magnetic resonance showed myocardial edema and intramyocardial late gadolinium enhancement. An abdominal ultrasound raised suspicion of a pheochromocytoma due to an abnormal mass with cystic areas found on the right suprarenal gland. Elevated urinary free catecholamines and fractionated metanephrines confirmed the diagnosis. Further on, a CT scan better identified the heterogeneous tumor and the patient was referred for a right laparoscopic adrenalectomy. Follow-up at 1 month reported full recovery of the sistolic function. The particularity of the case is represented by the difficulty of diagnosis of adrenergic myocarditis, as well as the management of cardiogenic shock induced by it.

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Development of a new micellar formulation of carvedilol and curcumin to enhance blood pressure reduction in a spontaneously hypertensive rat model

Santander Plantamura,

Allo,

Riedel

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Carvedilol Inhibits Matrix Metalloproteinase-2 Activation in Experimental Autoimmune Myocarditis: Possibilities of Cardioprotective Application

Cited by 14 publications

References 33 publications

HMG-CoA Reductase Inhibitor, Simvastatin Is Effective in Decreasing Degree of Myocarditis by Inhibiting Metalloproteinases Activation

HMG-CoA Reductase Inhibitor, Simvastatin Is Effective in Decreasing Degree of Myocarditis by Inhibiting Metalloproteinases Activation

Management of a rare case of adrenergic myocarditis complicated with cardiogenic shock

Development of a new micellar formulation of carvedilol and curcumin to enhance blood pressure reduction in a spontaneously hypertensive rat model

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