CUPRAC-Reactive Advanced Glycation End Products as Prognostic Markers of Human Acute Myocardial Infarction

Bayarsaikhan, Govigerel; Bayarsaikhan, Delger; Oh, Pyung Chun; Kang, Woong Chol; Lee, Bong-Hee

doi:10.3390/antiox10030434

Cited by 5 publications

(2 citation statements)

References 56 publications

(64 reference statements)

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“…There is consensus that the activated microglia is an important key mediator of proinflammatory and neurotoxic factors involved in the progression of PD and AD. These proinflammatory and neurotoxic factors include cytokines like interleukin-6 (IL-6) and interleukin-1β (IL-1β), the tumor necrosis factor-α (TNF-α) and ROS, consequently contributing to oxidative stress (Bayarsaikhan et al, 2015).…”

Section: Oxidative Stressmentioning

confidence: 99%

Metabolic syndrome and neuroprotection

Pacheco,

Matilde Otero-Losada

2023

Interamerican Journal of Health Sciences

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Introduction. Over the years, the prevalence of metabolic syndrome has increased dramatically in developing countries as a major byproduct of industrialization. Many factors, such as the consumption of high-calorie diets and a sedentary lifestyle, favor the spread of this disorder. Without a doubt, the massive and still growing incidence of metabolic syndrome places this epidemic as an important public health problem. Metabolic syndrome is also a neurological and psychiatric risk factor. In this work, an exploratory review of literature on the topic will be carried out. In this work, we review the information regarding what is known about metabolic syndrome beyond its classic association with cardiovascular disease and type 2 diabetes mellitus, since metabolic syndrome also represents a risk factor for nervous tissue and a threat neuronal function. First, we present some essential concepts of the pathophysiology of metabolic syndrome. Secondly, we explore some neuroprotective approaches in metabolic syndrome related to cerebral hypoxia. Goals. Update, exploratory review, and synthesize the literature regarding the neurological impact of metabolic syndrome, beyond its classic association with cardiovascular disease and type 2 diabetes mellitus. Define and review essential concepts of the pathophysiology of metabolic syndrome. Explore neuroprevention and neuroprotection strategies in metabolic syndrome related to therapeutic cerebral hypoxia. Material and methods. An exploratory survey of scientific literature from the period January 1989-November 2022 was carried out. Selection/inclusion criteria: scientific publications containing data and exploratory information on metabolic syndrome and neurological comorbidity and possible neurotherapeutic approaches. Pathophysiology. The metabolic pathways characteristically impaired in metabolic syndrome lead to hyperglycemia, insulin resistance, inflammation and hypoxia, all closely related to a generalized pro-oxidative state. Oxidative stress is well known to cause the destruction of cellular structures and tissue architecture. Disruption of redox homeostasis and oxidative stress alter the macromolecular matrix of nuclear genetic material, lipids and proteins, which in turn alters biochemical pathways necessary for normal cellular function. Neuroprotection. Different neuroprotective strategies are discussed that involve lifestyle changes, medications aimed at mitigating the cardinal symptoms of metabolic syndrome, and treatments aimed at reducing oxidative stress. It is well known that routine physical exercise, particularly aerobic activity, and a complete and balanced diet are key factors in preventing metabolic syndrome. However, pharmacological control of the metabolic syndrome as a whole and the corresponding hypertension, dyslipidemia and endothelial injury contribute to the improvement of neuronal health. Conclusion. The development of metabolic syndrome is presented as a risk factor for the development and/or exacerbation of neurological disorders. Therapeutic strategies include multidisciplinary approaches aimed at addressing, in a concerted manner, different pathways involved in its pathophysiology.

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Section: Oxidative Stressmentioning

confidence: 99%

Metabolic syndrome and neuroprotection

Pacheco,

Matilde Otero-Losada

2023

Interamerican Journal of Health Sciences

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“…AGEs play a central role in biomarkers for a variety of diseases, including neurodegenerative disorders, diabetes and diabetes-induced organ failures, alcoholic liver and brain damages, and others [ 19 , 20 , 21 ]. In addition, AGEs were observed in the hearts of humans and animals with acute myocardial infarction, and the increased activation of RAGE by AGEs showed increases in cell apoptosis through different biochemical pathways such as oxidative stress and hyper responsiveness to the macrophages during inflammation [ 22 , 23 , 24 , 25 ].…”

Section: Introductionmentioning

confidence: 99%

A Study on the Protective Effect of sRAGE-MSCs in a Rodent Reperfusion Model of Myocardial Infarction

Bayarsaikhan

Lee

et al. 2022

IJMS

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Acute myocardial infarction (AMI) is one of the major leading causes of death in humans globally. Recently, increased levels of recruited macrophages and AGE-albumin were observed in the hearts of humans and animals with acute myocardial infarction. Thus, the purposes of this study were to investigate whether the elevated levels of AGE-albumin from activated macrophage cells are implicated in ischemia-induced cardiomyocyte death and to develop therapeutic strategies for AMI based on its underlying molecular mechanisms with respect to AGEs. The present study demonstrated that activated macrophages and AGE-albumin were observed in heart tissues obtained from humans and rats with AMI incidences. In the cellular model of AMI, it was found that increased expression of AGE-albumin was shown to be co-localized with macrophages, and the presence of AGE-albumin led to increased expression of RAGE through the mitogen-activated protein kinase pathway. After revealing cardiomyocyte apoptosis induced by toxicity of the AGE-RAGE system, sRAGE-secreting MSCs were generated using the CRISPR/Cas9 platform to investigate the therapeutic effects of sRAGE-MSCs in an AMI rat model. Gene-edited sRAGE-MSCs showed greater therapeutic effects against AMI pathogenesis in rat models compared to mock MSCs, and promising results of the functional improvement of stem cells could result in significant improvements in the clinical management of cardiovascular diseases.

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Clinical Efficacy of Ulinastatin Combined with Meglumine Adenosine Cyclophosphate in the Treatment of Acute Myocardial Infarction

Zhang

Sun

et al. 2022

Computational and Mathematical Methods in Medicine

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Ulinastatin, a common adjuvant drug in the clinical treatment of acute circulatory failure, has a good effect on various inflammatory diseases. In this study, we aim to explore the clinical efficacy of ulinastatin combined with meglumine adenosine cyclophosphate in patients with acute myocardial infarction (AMI) and its effect on cardiac function and endothelial function of patients. 100 AMI patients treated in our hospital (February 2020-October 2020) were randomly chosen and divided into group J and group Q, with 50 cases in each group. Group Q was treated with meglumine adenosine cyclophosphate only, while group J was treated with ulinastatin combined with meglumine adenosine cyclophosphate to compare the treatment efficiency, cardiac structure indexes, cardiac systolic function, blood lipid levels, vascular endothelial function, QLI (quality of life) scores, BI indexes, and FMA (motor function) scores between the two groups. The treatment efficiency, QLI score, BI index, and FMA score in group J were notably higher compared with group Q ( P < 0.05 ). The cardiac structure indexes, cardiac systolic function, blood lipid level, and vascular endothelial function in group J were notably better compared with group Q ( P < 0.05 ). Ulinastatin combined with meglumine adenosine cyclophosphate can obviously enhance the therapeutic effect of AMI patients and improve the endothelial function and cardiac function of patients, which is very promising in this medical area.

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CUPRAC-Reactive Advanced Glycation End Products as Prognostic Markers of Human Acute Myocardial Infarction

Cited by 5 publications

References 56 publications

Metabolic syndrome and neuroprotection

Metabolic syndrome and neuroprotection

A Study on the Protective Effect of sRAGE-MSCs in a Rodent Reperfusion Model of Myocardial Infarction

Clinical Efficacy of Ulinastatin Combined with Meglumine Adenosine Cyclophosphate in the Treatment of Acute Myocardial Infarction

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