Ghrelin/GHSR-1a promotes angiogenesis after myocardial infarction through the glycolytic process.

Background: Therapeutic angiogenesis has demonstrated efficacy in revascularizing ischemic heart tissue and reducing the progression of cardiac remodeling following myocardial infarction. Recent studies have highlighted the significance of the glycolytic process in maintaining endothelial cell function and cardiac homeostasis. However, the specific role of glycolysis in angiogenesis post-myocardial infarction remains poorly understood.

Research progress of ghrelin on cardiovascular disease.

Ghrelin, a 28-aminoacid peptide, was isolated from the human and rat stomach and identified in 1999 as an endogenous ligand for the growth hormone secretagogue-receptor (GHS-R). In addition to stimulating appetite and regulating energy balance, ghrelin and its receptor GHS-R1a have a direct effect on the cardiovascular system. In recent years, it has been shown that ghrelin exerts cardioprotective effects, including the modulation of sympathetic activity and hypertension, enhancement of the vascular activity and angiogenesis, inhibition of arrhythmias, reduction in heart failure and inhibition of cardiac remodeling after myocardial infarction (MI).

The new mechanism of Ghrelin/GHSR-1a on autophagy regulation.

Autophagy is associated with several diseases. In recent years, accumulating evidence has suggested that ghrelin pathway exerts a protective effect by regulating autophagy. This review aims to assess the potential role and use of ghrelin as a new treatment for obesity, cardiovascular diseases, nonalcoholic fatty liver disease (NFALD), neurodegenerative diseases, and tissue damage associated with autophagy.

Effects of Traditional Chinese Medicine Shensong Yangxin Capsules on Heart Rhythm and Function in Congestive Heart Failure Patients with Frequent Ventricular Premature Complexes: A Randomized, Double-blind, Multicenter Clinical Trial.

Background: Pharmacological therapy for congestive heart failure (CHF) with ventricular arrhythmia is limited. In the study, our aim was to evaluate the effects of Chinese traditional medicine Shensong Yangxin capsules (SSYX) on heart rhythm and function in CHF patients with frequent ventricular premature complexes (VPCs).

Methods: This double-blind, placebo-controlled, multicenter study randomized 465 CHF patients with frequent VPCs to the SSYX (n = 232) and placebo groups (n = 233) for 12 weeks of treatment.

GHSR-1a is a novel pro-angiogenic and anti-remodeling target in rats after myocardial infarction.

Cardiac remodeling and subsequent heart failure is an increasing public health problem after myocardial infarction (MI). The aim of our research is to investigate whether gene therapy of growth hormone secretagogue receptor 1a may regulate cardiac remodeling and function after MI. Adenoviral vector expressing GHSR-1a or empty adeno-null was injected into rat peri-infarct myocardium after left anterior descending coronary artery ligation.

Advances of the interleukin-21 signaling pathway in immunity and angiogenesis.

Interleukin-21 (IL-21) and its receptor (IL-21R) are broadly expressed on human B cells, activated T cells and other myeloid cells. IL-21 cooperates with IL-6 and transforming growth factor-β to regulate T-cell differentiation. IL-21-mediated human B cell and dendritic cells differentiation requires signal transducer and activator of transcription 3 (STAT3), and also induces B-cell apoptosis dependents on the Toll-like receptor signal.

RETRACTED: Ghrelin protects infarcted myocardium by induction of autophagy and AMP-activated protein kinase pathway.

This article has been retracted: please see Elsevier Policy on Article Withdrawal (http://www.elsevier.com/locate/withdrawalpolicy).

Exosomes Mediate the Intercellular Communication after Myocardial Infarction.

The mechanisms of cardiac repair after myocardial infarction (MI) are complicated and not well-understood currently. It is known that exosomes are released from most cells, recognized as new candidates with important roles in intercellular and tissue-level communication. Cells can package proteins and RNA messages into exosome and secret to recipient cells, which regulate gene expression in recipient cells.

Potential new role of the GHSR-1a-mediated signaling pathway in cardiac remodeling after myocardial infarction (Review).

The gastrointestinal hormone ghrelin has important cardiovascular protective effects, however, its specific mechanisms are not yet completely understood. Recent studies have shown that the ghrelin receptor, growth hormone secretagogue receptor type 1a (GHSR-1a), regulates cell proliferation, apoptosis and inflammation-related signaling pathways. In human aortic endothelial cells, ghrelin activates NO production through AMP-activated protein kinase (AMPK) and Akt activation, and these effects can be blocked by knockdown of GHSR-1a.

Expression of ghrelin and its receptor in rats after coronary artery ligation.

Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial effects on cardiac function and ventricular remodeling. The present study aimed to investigate the expression of ghrelin and the growth hormone (GH) secretagogue receptor 1a (GHSR-1a), and the association with cardiac remodeling in rats with myocardial infarction (MI). Twenty-four hours after ligation of the anterior descending artery (LAD), adult male Sprague-Dawley rats were randomized to 3 d, 7 d and 28 d group.

Myocardial angiogenesis after chronic ghrelin treatment in a rat myocardial infarction model.

Ghrelin has a protective role in a rat model of myocardial infarction (MI), but the underlying mechanism is not clear. Here, we investigated the effects of ghrelin treatment on angiogenesis in an experimental rat MI model. Adult male Sprague-Dawley rats were subjected to MI by ligating the anterior descending coronary artery.

P75 neurotrophin receptor is a regulatory factor in sudden cardiac death with myocardial infarction.

Sudden cardiac death (SCD) is a major cause of morbidity and mortality in patients with coronary artery diseases and myocardial infarction (MI). Sympathetic stimulation and sympathetic neural remodeling are important in the generation of SCD in diseased heart. The balance of nerve growth factor (NGF) and semaphoring 3A determines the sympathetic innervation patterning.

Effects of ghrelin on Cx43 regulation and electrical remodeling after myocardial infarction in rats.

Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial effects on ventricular remodeling. In this study, we investigated whether ghrelin could decrease vulnerability to ventricular arrhythmias in rats with myocardial infarction and the possible mechanism. Twenty-four hours after ligation of the anterior descending artery, adult male Sprague-Dawley rats were randomized to ghrelin (100 μg/kg) and saline (control group) for 4 weeks.

[Cardioprotective effect and mechanism of post-infarction ventricular remodeling after self-assembling peptide and thermosensitive hydrogel implantation in rat myocardial infarction model].

Objective: To compare the cardioprotective effect of self-assembling peptide (RAD16-II) and thermosensitive hydrogel DPHP (Dex-PCL-HEMA/PNIPAAm) and investigate the optimal property of hydrogel for the treatment of myocardial infarction (MI).

Methods: MI model was induced by left anterior descending (LAD) coronary artery ligation in SD rats. The animals were randomized into three groups to receive RAD16-II hydrogel (n = 15), DPHP hydrogel (n = 15) or PBS (phosphate buffered saline; control group n = 15); sham-operated rats (n = 10), a suture was tied loosely around left coronary artery without ligating it.

Injectable hydrogel helps bone marrow-derived mononuclear cells restore infarcted myocardium.

Backgrounds: Experimental and clinical studies have suggested that cell implantation could improve cardiac function after myocardial infarction (MI). However, this technique was limited by decreased engraftment and survival of transplanted cells within the ischemic tissue. The present study was performed to investigate whether implantation of bone marrow-derived mononuclear cells (BMMNCs) encapsulated in hydrogel could increase cell engraftment and help to restore cardiac function of MI rabbits.

Ghrelin inhibits post-infarct myocardial remodeling and improves cardiac function through anti-inflammation effect.

Ghrelin is a novel growth hormone-releasing peptide, which has been shown to exert beneficial cardiac effects on chronic heart failure (CHF) recently. In this study, we attempted to investigate the mechanisms for the effect of ghrelin on ventricular remodeling following acute myocardial infarction (MI). Ligation of a coronary artery was used to create an MI in rats.

A novel peptide ghrelin inhibits neural remodeling after myocardial infarction in rats.

Ghrelin is a newly discovered peptide as an endogenous ligand for the growth hormone secretagogue receptor, and has been demonstrated to exert beneficial effect in the cardiovascular system. In the present study, we investigated whether ghrelin administration could inhibit cardiac neural remodeling and sympathetic hyperinnervation after myocardial infarction. Sprague-Dawley rats underwent coronary ligation to induce myocardial infarction and receiving ghrelin chronically (100 microg/kg s.