Therapeutic Potential of CXCR4/SDF-1 Axis in Acute Myocardial Infarction

2016 ◽  
Vol 1 (1) ◽  
pp. 20
Author(s):  
Shirin Hamedakbari Toosi ◽  
Javad Behravan ◽  
Asieh Heirani-Tabasi
2017 ◽  
Vol 3 ◽  
pp. 13
Author(s):  
Shirin Hamedakbari Toosi ◽  
Javad Behravan ◽  
Asieh Heirani-Tabasi

Acute Myocardial Infarction (AMI) is one of the mortal diseases which relate to heart and has many impacts on patients’ life. Stem cell therapy, including mesenchymal stem cells (MSCs), has emerged a promise treatment for patients with this disease. However, the inefficient migration and homing of MSCs have limited their therapeutic applications. It has been demonstrated that CXCR4/SDF-1 axis has a crucial role in cell migration and stem cell homing. So, many studies have conducted and currently are operating by novel methods to improve homing of MSCs by up-regulating the expression of CXCR4/SDF-1 axis to discover a proper cell therapy for AMI. CXCR4/SDF-1 axis triggers a variety of biological responses, such as directing cell migration, organogenesis, hematopoiesis, vascularization, and immune responses. Therefore, this axis might be a good candidate for manipulation with therapeutic purposes.


2014 ◽  
Vol 2014 ◽  
pp. 1-13
Author(s):  
Sheung-Fat Ko ◽  
Hon-Kan Yip ◽  
Steve Leu ◽  
Chen-Chang Lee ◽  
Jiunn-Jye Sheu ◽  
...  

This study investigates the therapeutic potential of intracoronary tacrolimus against acute myocardial infarction (AMI) in minipigs with serial cardiac magnetic resonance (CMR) and changes at histological and protein levels. Twelve minipigs subjected to permanent left anterior descending artery ligation were randomized as tac-treated group (n=6, with intracoronary tacrolimus treatment) and controls(n=6). CMR with cine and late gadolinium enhancement (LGE) studies were performed on postoperative days 2, 5, and 21. There were no significant differences in left ventricular function (LVF), contractility, and LGE between the two groups on day 2. On day 5, the tac-treated group showed a significantly higher ejection fraction, smaller infarct, and lower day-5/day-2 infarct ratio than controls. On day 21, the controls demonstrated further deterioration of LVF and infarct. Contrastingly, the tac-treated animals demonstrated preservation of LVF, contractility, significantly smaller infarct, and lower day-21/day-2 infarct ratios compared with those on day 5 and controls. Thein vivoCMR results were correlated within vitrofindings on histology, immunostaining, and Western blotting which revealed significantly less fibrosis, higher vascularities, less CD68+ and CD40+ inflammatory cells, lower expressions of inflammatory (MMP-9, NF-κB, and TNF-α), and apoptotic (Bax, Caspase-3, c-PARP) biomarkers, respectively, in tac-treated AMI minipigs than controls.


2005 ◽  
Vol 5 (4) ◽  
pp. 225-231 ◽  
Author(s):  
Teruo Inoue ◽  
Ryoichi Nishiki ◽  
Manabu Kageyama ◽  
Koichi Node

2022 ◽  
Vol 12 ◽  
Author(s):  
Tianwei Cui ◽  
Weiyu Liu ◽  
Chenghao Yu ◽  
Jianxun Ren ◽  
Yikui Li ◽  
...  

Acute myocardial infarction (AMI) is a condition with high morbidity and mortality, for which effective treatments are lacking. Allicin has been reported to exert therapeutic effects on AMI, but the underlying mechanisms of its action have not been fully elucidated. To investigate this, a rat model of AMI was generated by ligating the left anterior descending branch of the coronary artery. DL-propargylglycine (PAG), a specific hydrogen sulfide (H2S) synthetase inhibitor, was used to examine the effects of allicin on H2S production. Isolated coronary arteries and cardiomyocytes were assessed for vascular reactivity and cellular Ca2+ transport using a multiwire myography system and a cell-contraction-ion detection system, respectively. Allicin administration improved cardiac function and myocardial pathology, reduced myocardial enzyme levels, and increased H2S and H2S synthetase levels. Allicin administration resulted in concentration-dependent effects on coronary artery dilation, which were mediated by receptor-dependent Ca2+ channels, ATP-sensitive K+ channels, and sarcoplasmic reticulum (SR) Ca2+ release induced by the ryanodine receptor. Allicin administration improved Ca2+ homeostasis in cardiomyocytes by increasing cardiomyocyte contraction, Ca2+ transient amplitude, myofilament sensitivity, and SR Ca2+ content. Allicin also enhanced Ca2+ uptake via SR Ca2+-ATPase and Ca2+ removal via the Na+/Ca2+ exchanger, and it reduced SR Ca2+ leakage. Notably, the protective effects of allicin were partially attenuated by blockade of H2S production with PAG. Our findings provide novel evidence that allicin-induced production of H2S mediates coronary artery dilation and regulation of Ca2+ homeostasis in AMI. Our study presents a novel mechanistic insight into the anti-AMI effects of allicin and highlights the therapeutic potential of this compound.


2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Rachel Pathimagaraj

Coronary occlusion promotes a state of ischaemia that results in myocardial infarction; it  is  a  major  cause  of  mortality  accounting  for  one  hospital  admission  every  three minutes. At the site of infarct, sterile inflammation is initiated due to pro-inflammatory secretions from cardiac and innate immune cells. The focus of this review is to explore the role of a newly discovered innate immune complex, the nod-like receptor family pyrin domain containing 3 inflammasome. This review discusses the potential of this immune  complex  in  decreasing  the  proportion  of  functional  myocardium  during ischaemia   and   ischaemia-reperfusion   injury.   Due   to   the   central   role   of   this inflammasome  in  promoting  cardiac  dysfunction  following  an  acute  myocardial infarction,  the  risk  of  port-infarction  heart  failure  increases.  With  an  intention  of highlighting the importance of improving current management of patients with acute myocardial  infarction,  this  review  addresses  novel  therapeutic  agents  that  have demonstrated  cardioprotective  outcomes  in  recent  studies.  This  follows  discussion concerning the therapeutic potential of these agents, intending to form the basis of heart failure therapy.


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