Expression of vascular endothelial growth factor in cardiac repair: Signaling mechanisms mediating vascular protective effects

Yang, Zefu; Jian-ping, Wan; Pan, Wei; Zou, Jun

doi:10.1016/j.ijbiomac.2018.02.111

Cited by 8 publications

(5 citation statements)

References 27 publications

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“…Although ischemia leads to endogenous myocardial angiogenesis, it cannot reach the effect to maintain normal capillary density [130]. Experiments conducted on rat models reveal that serum VEGF-A levels are positively associated with increased microvessel density in the infarcted area, suggesting VEGF-A role in myocardial remodeling and angiogenesis [131][132][133][134][135]. There is compelling evidence that patients with MI have high serum levels of VEGF-A [136].…”

Section: Ischemic Heart Diseasementioning

confidence: 99%

“…Ischemic heart disease: →Myocardial infarction ↑ microvessel density in the infarcted area, myocardial remodeling angiogenesis, neovascularization, destabilization of inflamed plaques. [131][132][133][134][135][136][137] →Stroke ↑ vasodilation, vascular permeability, endothelial cells migration, dissociation of smooth muscle cells, loosening of the extracellular matrix. [146] Atherosclerosis: →Atherothrombosis ↓ vascular toxicity, arterial thrombosis.…”

Section: Cardiovascular Diseases Vegf-a Effects Referencesmentioning

confidence: 99%

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VEGF-A in Cardiomyocytes and Heart Diseases

Braile

Marcella

Cristinziano

et al. 2020

IJMS

176

107

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The vascular endothelial growth factor (VEGF), a homodimeric vasoactive glycoprotein, is the key mediator of angiogenesis. Angiogenesis, the formation of new blood vessels, is responsible for a wide variety of physio/pathological processes, including cardiovascular diseases (CVD). Cardiomyocytes (CM), the main cell type present in the heart, are the source and target of VEGF-A and express its receptors, VEGFR1 and VEGFR2, on their cell surface. The relationship between VEGF-A and the heart is double-sided. On the one hand, VEGF-A activates CM, inducing morphogenesis, contractility and wound healing. On the other hand, VEGF-A is produced by CM during inflammation, mechanical stress and cytokine stimulation. Moreover, high concentrations of VEGF-A have been found in patients affected by different CVD, and are often correlated with an unfavorable prognosis and disease severity. In this review, we summarized the current knowledge about the expression and effects of VEGF-A on CM and the role of VEGF-A in CVD, which are the most important cause of disability and premature death worldwide. Based on clinical studies on angiogenesis therapy conducted to date, it is possible to think that the control of angiogenesis and VEGF-A can lead to better quality and span of life of patients with heart disease.

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Section: Ischemic Heart Diseasementioning

confidence: 99%

Section: Cardiovascular Diseases Vegf-a Effects Referencesmentioning

confidence: 99%

VEGF-A in Cardiomyocytes and Heart Diseases

Braile

Marcella

Cristinziano

et al. 2020

IJMS

176

107

View full text Add to dashboard Cite

show abstract

“…Many experiments have shown that the level of VEGF is positively correlated with an increase in microvessel density in the infarct area, which suggests that VEGF plays a role in myocardial remodeling and angiogenesis ( 31 , 32 ). Although ischemia results in endogenous myocardial angiogenesis, it does not have the effect of maintaining normal capillary density ( 33 ).…”

Section: Discussionmentioning

confidence: 99%

Cardiac Repair With Echocardiography-Guided Multiple Percutaneous Left Ventricular Intramyocardial Injection of hiPSC-CMs After Myocardial Infarction

Wang²,

Qin

et al. 2021

Front. Cardiovasc. Med.

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Objective: We investigated the potency of cardiac repair based on echocardiography-guided multiple percutaneous left ventricular intramyocardial injection of human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) after myocardial infarction (MI).Methods: Mice with surgically induced MI were randomly divided into three groups (n = 8 in each group) and subjected to echocardiography-guided percutaneous left ventricular infarcted border injection of hiPSC-CMs (single dose; 10 μl 3 × 105 cells) or repeated injections of hiPSC-CMs at post-MI weeks 1 and 2 (multiple doses). The sham group of animals underwent all surgical procedures necessary for MI induction except for ligation. Then 4 weeks after MI, heart function was measured with transthoracic echocardiography. Engraftment was evaluated through the detection of human-specific cardiac troponin T. Infarct size and collagen volume were calculated with Sirius Red/Fast Green staining. Angiogenesis was evaluated with isolectin B4 staining. Cardiac remodeling was evaluated from the cardiomyocyte minimal fiber diameter in the infarcted border zone. Apoptosis was detected via TdT-mediated dUTP Nick-End Labeling (TUNEL) staining in cardiomyocytes from the infarcted border zone.Results: No mice died after echocardiography-guided percutaneous left ventricular intramyocardial injection. hiPSC-CMs were about nine-fold higher in the multiple-dose group at week 4 compared to the single-dose group. Multiple-dose transplantation was associated with significant improvement in left ventricular function, infarct size, angiogenesis, cardiac remodeling, and cardiomyocyte apoptosis.Conclusion: Echocardiography-guided multiple percutaneous left ventricular intramyocardial injection is a feasible, satisfactory, repeatable, relatively less invasive, and effective method of delivering cell therapy. The delivery of hiPSC-CMs indicates a novel therapy for MI.

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“…Аналогічна картина показана і в експерименті Yang і співавт. [17]. Сироватковий вміст СЕФР у щурів збільшувався на 105,3, 260, 378,2 і 271,3% від початку ГІМ на 3, 6, 9 і 12-й день відповідно.…”

Section: результати та їх обговоренняunclassified