Pathological Ventricular Remodeling

Burchfield, Jana; Xie, Min; Hill, Joseph A.

doi:10.1161/circulationaha.113.001878

Cited by 646 publications

(536 citation statements)

References 196 publications

(205 reference statements)

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“…Myocardial remodeling and heart function abnormalities after AMI affect patients' prognosis and living quality (Burchfield et al 2013). AMI results in scar formation, which can enhance the local contractility and prevent the heart from burst.…”

Section: Introductionmentioning

confidence: 99%

Exogenous BMP-7 Facilitates the Recovery of Cardiac Function after Acute Myocardial Infarction through Counteracting TGF-<i>β</i>1 Signaling Pathway

Xiao

et al. 2018

Tohoku J. Exp. Med.

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Myocardial fibrosis after acute myocardial infarction (AMI) is one of the main causes of myocardial remodeling and heart function abnormalities. Bone morphogenetic protein-7 (BMP-7) has been reported to play essential roles in anti-fibrosis. In this study, we demonstrated the role of exogenous BMP-7 on myocardial fibrosis and heart function recovery after AMI. A rat model of AMI was established via ligation of the left anterior descending coronary artery (LAD). Twenty rats were grouped into sham group which underwent chest open operation, but did not receive LAD ligation. Another 40 rats underwent LAD ligation were randomly grouped into saline-treated group (n = 20) and BMP-7-treated group (n = 20) which received saline treatment or exogenous BMP-7 treatment for 14 days, respectively. Two weeks after LAD ligation, the survival rate of BMP-7-treated AMI group was significantly improved compared to the saline group. Moreover, the cardiac function was preserved as shown by echocardiography examination, and the infarcted size was limited upon BMP-7 treatment. In addition, we investigated the role of TGF-β1 signaling pathway in BMP-7-mediated cardioprotective effects by analyzing the expression levels of TGF-β1, Smad 2 and Smad 3 in the infarct zone, border zone, and non-infarct zone. Western blot and quantitative PCR results suggested that BMP-7 attenuated myocardial fibrosis through counteracting TGF-β1 signaling pathway, thereby exerting cardioprotective effects. In conclusion, our data provide a potential therapeutic direction for preserving cardiac function and improving prognosis of AMI patients.

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Section: Introductionmentioning

confidence: 99%

Exogenous BMP-7 Facilitates the Recovery of Cardiac Function after Acute Myocardial Infarction through Counteracting TGF-<i>β</i>1 Signaling Pathway

Xiao

et al. 2018

Tohoku J. Exp. Med.

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“…1,2 Left ventricular remodeling is a complex process involving cardiac myocyte growth and death, vascular rarefaction, cardiac fibrosis, inflammation, alterations in cardiac energetics, and electrophysiological remodeling. Recently, several endogenous negative regulators of cardiac hypertrophy have been discovered, which are basally inactive and becomes activated in response to a pathological stimulus.…”

Section: See Related Article Pp 86-98mentioning

confidence: 99%

Regulators of G-Protein Signaling 10 and Heart Failure

et al. 2016

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“…LVR is a process of gradual cardiac enlargement, dysfunction, and typical molecular changes such as increased cell death, collagen accumulation, and oxidative stress. Cell death is the ‘primum movens’ of the process 2. New insights in the pathobiology of myocardial ischemic injury suggest that myocyte loss during the acute stage involves both apoptotic and non‐apoptotic cell death, thus enabling the development of new pharmacological agents 3.…”

Section: Introductionmentioning

confidence: 99%

The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction

Varela¹,

Mavroidis

Katsimpoulas³

et al. 2017

ESC Heart Failure

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AimRasagiline mesylate (N‐propargyl‐1 (R)‐aminoindan) (RG) is a selective, potent irreversible inhibitor of monoamine oxidase‐B with cardioprotective and anti‐apoptotic properties. We investigated whether it could be cardioprotective in a rat model undergoing experimental myocardial infarction (MI) by permanent ligation of the left anterior descending coronary artery.Methods and resultsRG was administered, intraperitoneally, for 28 days (2 mg/kg) starting 24 h after MI induction. Echocardiography analysis revealed a significant reduction in left ventricular end‐systolic and diastolic dimensions and preserved fractional shortening in RG‐treated compared with normal saline group at 28 days post‐MI (31.6 ± 2.3 vs. 19.6 ± 1.8, P < 0.0001), respectively. Treatment with RG prevented tissue fibrosis as indicated by interstitial collagen estimation by immunofluorescence staining and hydroxyproline content and attenuated the number of apoptotic myocytes in the border zone (65%) as indicated by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Caspase 3 relative protein levels were significantly decreased in the non‐infarcted myocardium. Markedly decreased malondialdehyde levels in the border zone indicate a reduction in tissue oxidative stress.ConclusionsOur study demonstrates a positive effect of RG in the post‐MI period with a significant attenuation in cardiac remodelling.

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Pathological Ventricular Remodeling

Cited by 646 publications

References 196 publications

Exogenous BMP-7 Facilitates the Recovery of Cardiac Function after Acute Myocardial Infarction through Counteracting TGF-<i>β</i>1 Signaling Pathway

Exogenous BMP-7 Facilitates the Recovery of Cardiac Function after Acute Myocardial Infarction through Counteracting TGF-<i>β</i>1 Signaling Pathway

Regulators of G-Protein Signaling 10 and Heart Failure

The neuroprotective agent Rasagiline mesylate attenuates cardiac remodeling after experimental myocardial infarction

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