Cardiac remodeling by fibrous tissue after infarction in rats

Sun, Yao; Zhang, John Q.; Zhang, Jiakun; Lamparter, Steffen

doi:10.1067/mlc.2000.105971

Cited by 159 publications

(120 citation statements)

References 27 publications

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“…Heart failure is an unfavorable consequence of myocardial remodelling after AMI (Sun, 2009). Cardiac structural remodelling is associated with inflammatory reactions, followed by scar formation in the infarcted area as well as changes in the non-infarcted myocardium, including interstitial fibrosis and vascular remodeling (Sun et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Park

Yoon

et al. 2011

Exp Mol Med

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Cardiac lymphatic system in the remodeling after acute myocardial infarction (AMI) has been overlooked. We wanted to investigate the role of bone marrow-derived endothelial progenitor cells (EPCs) and their contribution to lymphatic distribution in myocardial remodeling after AMI. Mouse (C57bl/6J) MI models were created by ligation of the left anterior descending coronary artery and were treated with phosphate buffered saline (PBS) or EPCs. Real-time RT-PCR with 2-to 4-week myocardial tissue samples revealed that lymphangiogenetic factors such as vascular endothelial growth factor (VEGF)-C (8.5 fold, P ＜ 0.05), VEGF-D (6.1 fold, P ＜ 0.05), Lyve-1 (15 fold, P ＜ 0.05), and Prox-1 (11 fold, P ＜ 0.05) were expressed at significantly higher levels in the PBS group than the EPC group. The PBS group also showed a significantly higher density of lymphatic vessels in the peri-infarction area. Echocardiography showed that from 2 weeks after the treatment, left ventricle (LV) dimensions at both systole and diastole were significantly smaller in the EPC group than in the PBS group (P ＜ 0.01) and LV fractional shortening was higher in the EPC group accordingly (P ＜ 0.01). Lymphangiogenic markers increased in a mouse MI model. EPC transplantation decreased lymphangiogenesis and adverse ventricular remodeling after AMI. These novel findings suggest that new lymphatic vessels may be formed in severely damaged myocardium, and may be involved in adverse myocardial remodeling after AMI.

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Section: Introductionmentioning

confidence: 99%

Endothelial progenitor cell transplantation decreases lymphangiogenesis and adverse myocardial remodeling in a mouse model of acute myocardial infarction

Park

Yoon

et al. 2011

Exp Mol Med

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“…TGF-1 mRNA expression significantly increases at day 3 and gradually decreases from days 7 to 28, even though their expression levels are still higher than controls [29]. In addition, Schnoor and colleagues have recently demonstrated that macrophages contain mRNAs for a large number of collagens (particularly collagen VI) and fibronectin [30].…”

Section: Multi-scalementioning

confidence: 99%

Multi-Scale Modeling and Analysis of Left Ventricular Remodeling Post Myocardial Infarction: Integration of Experimental and Computational Approaches

Jin¹,

Lindsey²

2010

Application of Machine Learning

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Progressive remodeling of the left ventricle (LV) following myocardial infarction (MI) involves spatiotemporal interactions among multiple cell types and the extracellular matrix environment. Despite the extensive experimental studies designed to elucidate the regulatory mechanisms, there is a growing recognition that the complexity of LV remodeling precludes the efficient identification of early diagnostic indicators after myocardial infarction. Currently, systemic approaches are needed to reduce this complexity. Previous studies in other systems demonstrate that establishing a multi-scale analytical model of LV remodeling response to MI will likely help in the development of prognostic therapies. In this review, we discuss the current approaches used for mathematical modeling of the LV, advantages and disadvantages of the approaches, and methods used to validate these models.

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“…Au nombre de quatre (TIMP-1 à -4), seule la TIMP-4 est plus ou moins spécifique du coeur [18]. Les données concernant l'expression des TIMP dans le postinfarctus sont disparates: on observe généralement des augmentations de l'expression de leurs ARNm [19][20][21][22], mais les résultats divergent au niveau protéique [23][24][25][26]. Cependant, une baisse des taux protéiques des TIMP est le plus souvent rapportée, qui reflète une régu-lation post-transcriptionnelle importante.…”

Section: Remodelage De La Matrice Extracellulaireunclassified

“…La fibrose substitutive tente de maintenir l'intégrité structurale de la zone infarcie à la suite de la nécrose et de la détersion des myocytes. Les myofibroblastes apparaissent dans la zone infarcie dès le 3 e jour et se colocalisent avec l'expression des collagènes I et III [22]. Les taux de collagène sont augmentés surtout dans la zone infarcie, mais aussi dans le myocarde non infarci.…”

Section: Remodelage De La Matrice Extracellulaireunclassified

“…Les taux de collagène sont augmentés surtout dans la zone infarcie, mais aussi dans le myocarde non infarci. On observe dès le 3 e jour après l'infarctus une augmentation des ARNm, avec un pic au 7 e jour et une diminution ensuite [22,27]. L'accumulation de collagène est donc plus tardive que sa dégradation, le décalage représentant la période de risque de rupture du ventricule.…”

Section: Remodelage De La Matrice Extracellulaireunclassified

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