Cardiac μ-opioid receptor contributes to opioid-induced cardioprotection in chronic heart failure

He, Songqing; Jin, Shiyun; Yang, Wei; Pan, Yuzhen; Huang, Jun; Zhang, S.J.; Zhang, Liang; Zhang, Y.

doi:10.1016/j.bja.2017.11.110

Cited by 32 publications

(22 citation statements)

References 36 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In ischemic pre-conditioning rodent models, morphine exerted cardio-protective effects, as shown by reduced infarct size and area at risk [ 46 ]. Unfortunately, numerous studies have only been performed ex vivo in isolated hearts [ 52 , 53 , 54 , 55 ] or in vitro [ 56 ]. This complicates a direct extrapolation to the in vivo situation and particularly to an inflammatory disease as CVB3-induced myocarditis in which the immune system plays a predominant role.…”

Section: Resultsmentioning

confidence: 99%

Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Pappritz

Linthout

2020

Biology

View full text Add to dashboard Cite

Myocarditis is an inflammatory disorder of the heart predominantly caused by infectious agents. Since more than sixty years, the Coxsackievirus B3 (CVB3)-induced myocarditis mouse model is the experimental model used to investigate viral myocarditis. The pathogenesis of viral myocarditis is conceptually a multiphase process, initiated by the infection of cardiomyocytes, followed by activation of the immune system, and resulting in myocardial fibrosis and left ventricular dysfunction. In parallel to the direct infection of the heart, CVB3 replicates in lymphatic organs such as the pancreas. Due to infection of the pancreas, the model of experimental CVB3-induced myocarditis is estimated as a severe burden for the challenged animals. Application of analgesics in frame of the animal welfare act (European directive 2010/63/EU) is more and more becoming a matter of debate. For this purpose, we summarized published studies for 13 different opioids and discussed their potential impact on CVB3-induced myocarditis. In addition, with this summary we also want to provide guidance for researchers beyond the myocarditis field to estimate the impact of opioids on the immune system for their specific model. In the literature, both immunosuppressive as well as immune-activating effects of opioids have been described, but examinations in experimental CVB3-induced myocarditis have still not been reported so far. Based on the existing publications, administration of opioids in experimental CVB3-induced myocarditis might result in more severe disease progression, including higher mortality, or a less pronounced myocarditis model, failing to be used for the establishment of new treatment options. Taken together, the applicability of opioids in experimental CVB3-induced myocarditis and in inflammatory models in general needs to be carefully evaluated and further investigated.

show abstract

Section: Resultsmentioning

confidence: 99%

Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Pappritz

Linthout

2020

Biology

View full text Add to dashboard Cite

show abstract

“…Meanwhile, activation of the k receptors directly participates in the stimulation of the NOS/NO signaling pathway [107] and involve protein kinases pathways as AKT/Pi3K and ERK/MAPK [108]. Morphine or remifentanil administration before myocardial IRI can induce cardioprotection through the µ receptors via the ERK/GSK-3b signaling pathway [109]. This receptor has also been postulated as a potential therapeutic target for opioid-induced protection during heart failure [105,109].…”

Section: Extra-renal Opioid Preconditioning Mechanismsmentioning

confidence: 99%

“…Morphine or remifentanil administration before myocardial IRI can induce cardioprotection through the µ receptors via the ERK/GSK-3b signaling pathway [109]. This receptor has also been postulated as a potential therapeutic target for opioid-induced protection during heart failure [105,109].…”

Section: Extra-renal Opioid Preconditioning Mechanismsmentioning

confidence: 99%

Opioids Preconditioning Upon Renal Function and Ischemia-Reperfusion Injury: A Narrative Review

et al. 2019

View full text Add to dashboard Cite

Kidneys have an important role in regulating water volume, blood pressure, secretion of hormones and acid-base and electrolyte balance. Kidney dysfunction derived from acute injury can, under certain conditions, progress to chronic kidney disease. In the late stages of kidney disease, treatment is limited to replacement therapy: Dialysis and transplantation. After renal transplant, grafts suffer from activation of immune cells and generation of oxidant molecules. Anesthetic preconditioning has emerged as a promising strategy to ameliorate ischemia reperfusion injury. This review compiles some significant aspects of renal physiology and discusses current understanding of the effects of anesthetic preconditioning upon renal function and ischemia reperfusion injury, focusing on opioids and its properties ameliorating renal injury. According to the available evidence, opioid preconditioning appears to reduce inflammation and reactive oxygen species generation after ischemia reperfusion. Therefore, opioid preconditioning represents a promising strategy to reduce renal ischemia reperfusion injury and, its application on current clinical practice could be beneficial in events such as acute renal injury and kidney transplantation.

show abstract

“…Research on opioid receptor activation in the adult myocardium has focused mainly on DOR and KOR while the contributions of MOR have mainly been ignored due to its low expression in healthy cardiac tissue [ 72 , 73 , 74 ]. However, MOR expression and its ligand-binding activity increase after ligation of the coronary artery in animal models and in isolated failing hearts [ 75 , 76 ]. Morphine or remifentanil administration before myocardial IRI induces MOR-mediated protection in failing hearts but not in healthy ones [ 76 ].…”

Section: Mechanisms Of Opioid Conditioning In the Heartmentioning

confidence: 99%

“…However, MOR expression and its ligand-binding activity increase after ligation of the coronary artery in animal models and in isolated failing hearts [ 75 , 76 ]. Morphine or remifentanil administration before myocardial IRI induces MOR-mediated protection in failing hearts but not in healthy ones [ 76 ]. These protective effects appear to be dependent on phosphorylation of ERK1/2 and glycogen synthase kinase 3-βdownstream of MOR activation.…”

Section: Mechanisms Of Opioid Conditioning In the Heartmentioning

confidence: 99%

Novel Roles of Non-Coding RNAs in Opioid Signaling and Cardioprotection

Melo

Ishida

Goldaraz

et al. 2018

ncRNA

View full text Add to dashboard Cite

Cardiovascular disease (CVD) is a significant cause of morbidity and mortality across the world. A large proportion of CVD deaths are secondary to coronary artery disease (CAD) and myocardial infarction (MI). Even though prevention is the best strategy to reduce risk factors associated with MI, the use of cardioprotective interventions aimed at improving patient outcomes is of great interest. Opioid conditioning has been shown to be effective in reducing myocardial ischemia-reperfusion injury (IRI) and cardiomyocyte death. However, the molecular mechanisms behind these effects are under investigation and could provide the basis for the development of novel therapeutic approaches in the treatment of CVD. Non-coding RNAs (ncRNAs), which are functional RNA molecules that do not translate into proteins, are critical modulators of cardiac gene expression during heart development and disease. Moreover, ncRNAs such as microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) are known to be induced by opioid receptor activation and regulate opioid signaling pathways. Recent advances in experimental and computational tools have accelerated the discovery and functional characterization of ncRNAs. In this study, we review the current understanding of the role of ncRNAs in opioid signaling and opioid-induced cardioprotection.

show abstract

Cardiac μ-opioid receptor contributes to opioid-induced cardioprotection in chronic heart failure

Abstract: Cardiac μ-opioid receptors were substantially up-regulated during heart failure, which increased DAMGO-induced cardioprotection against I/R injury.

Cited by 32 publications

References 36 publications

Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Opioid-Induced Immunomodulation: Consequences for the Experimental Coxsackievirus B3-Induced Myocarditis Model

Opioids Preconditioning Upon Renal Function and Ischemia-Reperfusion Injury: A Narrative Review

Novel Roles of Non-Coding RNAs in Opioid Signaling and Cardioprotection

Contact Info

Product

Resources

About