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

Lin, Yu-Hao; Liu, Haiqiong; Wang, Xianbao

doi:10.3892/ijmm.2020.4662

Cited by 13 publications

(12 citation statements)

References 93 publications

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“…A member of the epidermal growth factor family, neuregulin-1 (NRG-1) is crucial for the development of cardiomyocytes and cardiac regeneration. There are six isoforms, and each one has an EGF-like domain that is both required and sufficient to activate ErbB receptors and, thus, exerts essential biological activities [ 213 ]. Prior studies have shown the following: NRG1 undertakes anti-fibrotic and anti-remodeling actions in heart failure models, it protects myocardial cells from damage and it improves cardiac function [ 214 ].…”

Section: Resultsmentioning

confidence: 99%

From Classic to Modern Prognostic Biomarkers in Patients with Acute Myocardial Infarction

Stătescu

Anghel

Tudurachi

et al. 2022

IJMS

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Despite all the important advances in its diagnosis and treatment, acute myocardial infarction (AMI) is still one of the most prominent causes of morbidity and mortality worldwide. Early identification of patients at high risk of poor outcomes through the measurement of various biomarker concentrations might contribute to more accurate risk stratification and help to guide more individualized therapeutic strategies, thus improving prognoses. The aim of this article is to provide an overview of the role and applications of cardiac biomarkers in risk stratification and prognostic assessment for patients with myocardial infarction. Although there is no ideal biomarker that can provide prognostic information for risk assessment in patients with AMI, the results obtained in recent years are promising. Several novel biomarkers related to the pathophysiological processes found in patients with myocardial infarction, such as inflammation, neurohormonal activation, myocardial stress, myocardial necrosis, cardiac remodeling and vasoactive processes, have been identified; they may bring additional value for AMI prognosis when included in multi-biomarker strategies. Furthermore, the use of artificial intelligence algorithms for risk stratification and prognostic assessment in these patients may have an extremely important role in improving outcomes.

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Section: Resultsmentioning

confidence: 99%

From Classic to Modern Prognostic Biomarkers in Patients with Acute Myocardial Infarction

Stătescu

Anghel

Tudurachi

et al. 2022

IJMS

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“…Of note, activation and agonists of ErbB2 have been proposed as therapeutic approaches for heart disease. ErbB2 overexpression and activator (Neuregulin 1, NRG1) promote cardiac function and repair, particularly in myocardial infarction and heart failure [27,44,45]. More meaningfully, a phase II clinical trial demonstrated that NRG1 effectively improved cardiac function in patients with stable congestive heart failure [46].…”

Section: Discussionmentioning

confidence: 99%

Metformin alleviates ethanol-induced cardiomyocyte injury by activating AKT/Nrf2 signaling in an ErbB2-dependent manner

et al. 2023

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Background Metformin, a rst-line oral anti-diabetic drug, has recently been reported to exert protective effect on various cardiovascular diseases. However, the potential role of metformin in ethanol-induced cardiomyocyte injury is still unknown. Therefore, this study was aimed to investigate the effect of metformin on ethanol-induced cardiomyocyte injury and its underlying mechanism.Methods and Results H9c2 cardiomyocytes were exposed to ethanol for 24 h to establish an ethanolinduced cardiomyocyte injury model, and followed by treatment with metformin in the presence or absence of Lapatinib (an ErbB2 inhibition). CCK8 and LDH assays demonstrated that metformin suppressed cardiomyocyte apoptosis induced by ethanol exposure. Furthermore, the up-regulated expressions of apoptosis-related proteins (Bax and C-CAS-3) were also reduced by metformin. In addition, our results showed that metformin activated the AKT/Nrf2 pathway, and then promoted Nrf2 nuclear translocation and the transcription of its downstream antioxidant genes (HO-1, CAT and SOD2), thereby inhibiting oxidative stress. Interestingly, we found that ErbB2 expression was signi cantly inhibited in ethanol-treated cardiomyocyte, which was markedly reversed by metformin. In contrast, Lapatinib largely abrogated the activation of AKT/Nrf2 signaling by metformin, accompanied by the increases in oxidative stress and cardiomyocyte apoptosis,indicating that metformin prevented ethanol-induced cardiomyocyte injury in an ErbB2-dependent manner.Conclusions In summary, our study provides the rst evidence that metformin protects cardiomyocyte against ethanol-induced oxidative stress and apoptosis by activating ErbB2-mediated AKT/Nrf2 signaling. Thus, metformin may be a potential novel treatment approach for alcoholic cardiomyopathy.

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“…Activation of ErbB receptors prevents cardiomyopathy [ 132 , 133 ], while their inhibition causes HF in mice [ 134 , 135 , 136 , 137 ]. Neuregulin-1 is mainly synthesized and secreted by endocardial and microvascular endothelial cells in the heart [ 292 ]. Experimental studies and clinical trials demonstrated that recombinant human neuregulin-1 reversed ventricular remodeling and improved cardiac function in subjects with HF [ 293 , 294 , 295 , 296 , 297 ].…”

Section: Emerging Treatment Targeting Specific Mechanisms Of Diabetic...mentioning

confidence: 99%

Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice

et al. 2023

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Diabetic cardiomyopathy is characterized by abnormal myocardial structure or performance in the absence of coronary artery disease or significant valvular heart disease in patients with diabetes mellitus. The spectrum of diabetic cardiomyopathy ranges from subtle myocardial changes to myocardial fibrosis and diastolic function and finally to symptomatic heart failure. Except for sodium–glucose transport protein 2 inhibitors and possibly bariatric and metabolic surgery, there is currently no specific treatment for this distinct disease entity in patients with diabetes. The molecular mechanism of diabetic cardiomyopathy includes impaired nutrient-sensing signaling, dysregulated autophagy, impaired mitochondrial energetics, altered fuel utilization, oxidative stress and lipid peroxidation, advanced glycation end-products, inflammation, impaired calcium homeostasis, abnormal endothelial function and nitric oxide production, aberrant epidermal growth factor receptor signaling, the activation of the renin–angiotensin–aldosterone system and sympathetic hyperactivity, and extracellular matrix accumulation and fibrosis. Here, we summarize several important emerging treatments for diabetic cardiomyopathy targeting specific molecular mechanisms, with evidence from preclinical studies and clinical trials.

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

Cited by 13 publications

References 93 publications

From Classic to Modern Prognostic Biomarkers in Patients with Acute Myocardial Infarction

From Classic to Modern Prognostic Biomarkers in Patients with Acute Myocardial Infarction

Metformin alleviates ethanol-induced cardiomyocyte injury by activating AKT/Nrf2 signaling in an ErbB2-dependent manner

Emerging Therapy for Diabetic Cardiomyopathy: From Molecular Mechanism to Clinical Practice

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