Remote ischemic perconditioning attenuates adverse cardiac remodeling and preserves left ventricular function in a rat model of reperfused myocardial infarction

Pilz, Patrick M.; Hamza, Ouafa; Gidlöf, Olof; Gonçalves, Inês Fonseca; Tretter, Eva Verena; Trojanek, S; Abraham, Dietmar; Heber, Stefan; Haller, P; Podesser, Bruno K.; Kiss, Attila

doi:10.1016/j.ijcard.2019.03.003

Cited by 38 publications

(39 citation statements)

References 40 publications

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“…For conferring protection against IR injury, IP plays a key role in the alleviation of oxidative stress, inflammation and apoptosis through NO production and mitoKATP channels opening by salvage kinase pathways, including AKT, ERK1/2, 5' AMP-activated protein kinase (AMPK), protein kinase (PK)c and PKG (84)(85)(86). Of note, in vivo, IP promotes NRG-1 protein expression, as well as the upregulation/activation of ErbB3 and ErbB4, indicating that the cardioprotection may be mediated by the NRG-1/ErbB3 and ErbB4 signaling pathways, which has also recently been confirmed in ischemic local postconditioning (87).…”

Section: Involvement Of Nrg-1 In Conditioning Against Myocardial Ir Injurymentioning

confidence: 80%

Neuregulin‑1, a microvascular endothelial‑derived protein, protects against myocardial ischemia‑reperfusion injury (Review)

2020

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As regards acute myocardial infarction, great success has been achieved in therapies that reduce the effects of myocardial ischemic injury, while few interventions have achieved satisfactory outcomes for myocardial ischemia-reperfusion (IR) injury. Thus, new research is urgently required to achieve breakthroughs in promising treatments. Neuregulin-1 (NRG-1), which is an endothelium-derived protein and the ligand of ErbB receptors, exerts cardioprotective effects and is rapidly upregulated during IR. NRG-1/ErbB activates several downstream signaling pathways in response to myocardial IR injury. Previous studies have revealed the protective effects of NRG-1 during heart failure, and numerous experiments have explored the mechanisms underlying the NRG-1-induced cardioprotective effects against myocardial IR injury. In the present review, the progress made in the research of NRG-1 as a cardioprotective agent during IR and related conditionings is summarized. Furthermore, the potential benefits of NRG-1 against myocardial IR injury are listed with the prospective use of NRG-1 in clinical applications. Contents

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Section: Involvement Of Nrg-1 In Conditioning Against Myocardial Ir Injurymentioning

confidence: 80%

Neuregulin‑1, a microvascular endothelial‑derived protein, protects against myocardial ischemia‑reperfusion injury (Review)

2020

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“…A total of 30 male Sprague-Dawley rats (weight, 200-250 g) from Shanghai Animal Research Center (http://www.slarc.org.cn/slarcWebSite/homeIndex. action) were randomly divided into six groups (n=5/group) as follows: i) Healthy control group; ii) Sham operation group; iii) Myocardial infarction model group; iv) myocardial infarction + low-dose tetrandrine group (10 mg/kg); v) myocardial infarction + medium-dose tetrandrine group (50 mg/kg); and vi) myocardial infarction + high-dose tetrandrine group (80 mg/kg), according to a previous study (17). All rats were housed at 21±2˚C, 0.03% CO 2 , 30-70% relative humidity and 12/12 h light/dark cycle with free access to food and water.…”

Section: Methodsmentioning

confidence: 99%

Tetrandrine attenuates left ventricular dysfunction in rats with myocardial infarction

Zhao

et al. 2020

Exp Ther Med

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The present study aimed to determine whether tetrandrine could attenuate left ventricular dysfunction and remodeling in rats with myocardial infarction. Sprague-Dawley rats were randomly divided into six groups (n=5/group) as follows: i) Healthy control group; ii) sham operation group; iii) myocardial infarction model group; iv) myocardial infarction + low-dose tetrandrine group (10 mg/kg); v) myocardial infarction + medium-dose tetrandrine group (50 mg/kg); and vi) myocardial infarction + high-dose tetrandrine group (80 mg/kg). Left ventricular end-diastolic diameter (LVIDd), left ventricular end-systolic diameter (LVIDs), ejection fraction (EF%) and left ventricular fractional shortening rate (FS%) were measured using ultrasonography. The pathological changes were observed by hematoxylin and eosin (H&E) staining. Left ventricular tissue section TUNEL staining was also performed. Furthermore, the triglyceride (TG), total cholesterol (TC), high density lipoprotein (HDL) and low-density lipoprotein (LDL) in the arterial blood were examined by biochemical testing. Expression levels of intracellular Ca 2+ homeostasis-related proteins including ryanodine receptor calmodulin, CaM-dependent protein kinase IIδ, protein kinase A, FK506 binding protein 12.6 were measured using western blot analysis. Ultrasonography results showed that in the myocardial infarction model rats, the levels of LVIDd and LVIDs were significantly higher; however, the levels of EF% and FS% were lower compared with those in the sham operation group, which was alleviated by tetrandrine. H&E results showed that tetrandrine alleviated the pathological characteristics of myocardial infarction model rats. Furthermore, tetrandrine significantly inhibited myocardial cell apoptosis in rats with myocardial infarction. Tetrandrine significantly inhibited the levels of TG, TC and LDL and increased the levels of HDL in the arterial blood of rats with myocardial infarction. These findings revealed that tetrandrine could attenuate left ventricular dysfunction in rats with myocardial infarction, which might be associated with intracellular Ca 2+ homeostasis.

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“…Following MI-R injury, TNF-α deficiency exhibited attenuated chemokine expression and NF-κB activation in the infarcted heart resulting in reduced infarct size and improved cardiac function ( 102 ). Additional remote ischemic preconditioning prior to reperfusion attenuated the inflammatory response causing decreased levels of TNF-α and IL-1β accompanied with an improved LV function ( 103 ). Pharmacological treatment with morphine following MI-R injury was shown to decrease circulating TNF-α levels and reduce infarct size with concomitant improvement of LV function ( 104 ).…”

Section: Myocardial Ischemia–reperfusion Injurymentioning

confidence: 99%

Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies

Pluijmert

Atsma

Quax

2021

Front. Cardiovasc. Med.

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Following acute occlusion of a coronary artery causing myocardial ischemia and implementing first-line treatment involving rapid reperfusion, a dynamic and balanced inflammatory response is initiated to repair and remove damaged cells. Paradoxically, restoration of myocardial blood flow exacerbates cell damage as a result of myocardial ischemia–reperfusion (MI-R) injury, which eventually provokes accelerated apoptosis. In the end, the infarct size still corresponds to the subsequent risk of developing heart failure. Therefore, true understanding of the mechanisms regarding MI-R injury, and its contribution to cell damage and cell death, are of the utmost importance in the search for successful therapeutic interventions to finally prevent the onset of heart failure. This review focuses on the role of innate immunity, chemokines, cytokines, and inflammatory cells in all three overlapping phases following experimental, mainly murine, MI-R injury known as the inflammatory, reparative, and maturation phase. It provides a complete state-of-the-art overview including most current research of all post-ischemic processes and phases and additionally summarizes the use of immunomodulatory therapies translated into clinical practice.

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Remote ischemic perconditioning attenuates adverse cardiac remodeling and preserves left ventricular function in a rat model of reperfused myocardial infarction

Cited by 38 publications

References 40 publications

Neuregulin‑1, a microvascular endothelial‑derived protein, protects against myocardial ischemia‑reperfusion injury (Review)

Neuregulin‑1, a microvascular endothelial‑derived protein, protects against myocardial ischemia‑reperfusion injury (Review)

Tetrandrine attenuates left ventricular dysfunction in rats with myocardial infarction

Post-ischemic Myocardial Inflammatory Response: A Complex and Dynamic Process Susceptible to Immunomodulatory Therapies

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