The role of myeloperoxidase as a diagnostic and prognostic factor in cardiovascular pathology (acute coronary syndrome)

Myeloperoxidase is one of the key enzymes involved in oxidative stress and inflammation. Its elevated levels are determined in a wide range of both acute and chronic forms of cardiovascular diseases. The inflammation results in the release of the enzyme from the white blood cells to form products such as hypochlorous acid, which in turn can have a negative effect on the target proteins. Inconsistent evidence on the predictive role of this biomarker in diseases of the circulatory system generates scientific interest and provokes further research in this direction. The aim of this review is to analyze the scientific literature data on myeloperoxidase as a possible clinical use for the diagnosis and risk stratification of patients with саrdiovascular diseases. Materials and methods. Searching and generalization of data from leading specialized sources, which are indexed by scientific databases PubMed, SCOPUS, Web of Science. Results. The results of the studies indicate that myeloperoxidase is actively involved in the pathophysiology of cardiovascular diseases through participation in oxidative stress and inflammation, excessive production of proatherogenic lipoproteins, changes in nitric oxide activity, endothelial dysfunction, and due to the effect on the instability of atherosclerotic plaques. In patients with cardiovascular diseases, including ischemic heart disease, the concentration of the indicated protein is increased and is often associated with a poor prognosis, including an increased risk of mortality. Myeloperoxidase metabolites are often the factors that contribute to cell damage under conditions of ischemia. The review also considers the relationship of the enzyme with the development of restenosis and the effectiveness of revascularization after percutaneous coronary intervention. Conclusions. The presented data mainly define myeloperoxidase as a significant marker for predicting long-term follow-up results and the development of serious adverse cardiovascular events, mortality in patients with cardiovascular disease. At the same time, despite the great achievements in disclosing the complex effects of myeloperoxidase, inconsistency in the available results is noteworthy. This controversy necessitates further research to elucidate and reveal the full clinical potential of myeloperoxidase in patients with cardiovascular pathology.

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Perspectives of incretin mimetics in cardiovascular diseases

Brazilian Journal of Health and Biomedical Sciences ◽

10.12957/bjhbs.2021.59746 ◽

2021 ◽

Vol 20 (1) ◽

pp. 55-62

Author(s):

João Felipe R. Cardoso ◽

Célia Cohen ◽

Fernanda J. Medeiros ◽

Fabiano M. Serfaty ◽

Mario F. T. Neves

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Nutrient Intake ◽

Web Of Science ◽

Myocardial Function ◽

Eye Diseases ◽

Incretin Mimetics ◽

Increased Risk

Introduction: Type 2 Diabetes (DM2) is a chronic conditionassociated with an increased risk of cardiovascular diseases,neuropathies, nephropathies and eye diseases. Incretins (GIPand GLP-1) are hormones important to insulin secretion, andtheir actions are compromised in DM2 patients. Objectives:This review considers the opportunities and challenges ofusing incretin mimetics in the treatment of DM2. Methods:Bibliographic review referring to the period from 2000 to2020, in electronic databases such as Scielo, Lilacs, PubMed,Web of Science. Results: Incretins stimulate insulin secretionby the pancreas in response to nutrient intake, with a lowerpotential to cause hypoglycemia. In addition, they have acardioprotective role, reducing blood pressure, improvingendothelial and myocardial function, and their use has beenassociated with a reduction in the risk of cardiovascularevents, including cardiovascular mortality. Clinical trialswith GLP-1R agonists (GLP-1RA) reduced albuminuria, increasednatriuresis, and decreased oxidative stress. In addition,treatment with incretin mimetics reduced the occurrence ofthe main cardiovascular outcomes related to atherosclerosis,promoted weight loss and improved lipid profile. Conclusion:Studies show the important role of incretin mimetics in thepathophysiology and treatment of DM2, with significanteffects in the cardiovascular system. However, its use must beevaluated in relation to its safety and to in which individualsthe benefits outweigh the risks associated with the treatment.Thus, its clinical relevance depends on studies with long-termfollow-up of patients, with analysis of its impact on mortalityand on the development of micro and macrovascularcomplications.

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SIRT3: A New Regulator of Cardiovascular Diseases

Oxidative Medicine and Cellular Longevity ◽

10.1155/2018/7293861 ◽

2018 ◽

Vol 2018 ◽

pp. 1-11 ◽

Cited By ~ 25

Author(s):

Wei Sun ◽

Caixia Liu ◽

Qiuhui Chen ◽

Ning Liu ◽

Youyou Yan ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Mitochondrial Function ◽

Causes Of Death ◽

Cell Damage ◽

Heart Diseases ◽

Tca Cycle ◽

Metabolic Disturbances ◽

Glucose And Lipid Metabolism

Cardiovascular diseases (CVDs) are the leading causes of death worldwide, and defects in mitochondrial function contribute largely to the occurrence of CVDs. Recent studies suggest that sirtuin 3 (SIRT3), the mitochondrial NAD+-dependent deacetylase, may regulate mitochondrial function and biosynthetic pathways such as glucose and fatty acid metabolism and the tricarboxylic acid (TCA) cycle, oxidative stress, and apoptosis by reversible protein lysine deacetylation. SIRT3 regulates glucose and lipid metabolism and maintains myocardial ATP levels, which protects the heart from metabolic disturbances. SIRT3 can also protect cardiomyocytes from oxidative stress-mediated cell damage and block the development of cardiac hypertrophy. Recent reports show that SIRT3 is involved in the protection of several heart diseases. This review discusses the progress in SIRT3-related research and the role of SIRT3 in the prevention and treatment of CVDs.

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Unveiling the Role of Inflammation and Oxidative Stress on Age-Related Cardiovascular Diseases

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/1954398 ◽

2020 ◽

Vol 2020 ◽

pp. 1-20 ◽

Cited By ~ 10

Author(s):

Arthur José Pontes Oliveira de Almeida ◽

Mathania Silva de Almeida Rezende ◽

Sabine Helena Dantas ◽

Sonaly de Lima Silva ◽

Júlio César Pinheiro Lúcio de Oliveira ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Inflammatory Process ◽

Cell Damage ◽

Stressful Environment ◽

Age Related ◽

Cellular Components ◽

Global Population ◽

And Oxidative Stress

The global population above 60 years has been growing exponentially in the last decades, which is accompanied by an increase in the prevalence of age-related chronic diseases, highlighting cardiovascular diseases (CVDs), such as hypertension, atherosclerosis, and heart failure. Aging is the main risk factor for these diseases. Such susceptibility to disease is explained, at least in part, by the increase of oxidative stress, in which it damages cellular components such as proteins, DNA, and lipids. In addition, the chronic inflammatory process in aging “inflammaging” also contributes to cell damage, creating a stressful environment which drives to the development of CVDs. Taken together, it is possible to identify the molecular connection between oxidative stress and the inflammatory process, especially by the crosstalk between the transcription factors Nrf-2 and NF-κB which are mediated by redox signalling and are involved in aging. Therapies that control this process are key targets in the prevention/combat of age-related CVDs. In this review, we show the basics of inflammation and oxidative stress, including the crosstalk between them, and the implications on age-related CVDs.

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THE ROLE OF TRACE ELEMENT SELENIUM IN THE DEVELOPMENT OF CARDIOVASCULAR DISEASES

Inter Collegas ◽

10.35339/ic.6.2.77-81 ◽

2019 ◽

Vol 6 (2) ◽

pp. 77-81

Author(s):

Larysa Zhuravlyova ◽

Maryna Filonenko

Keyword(s):

Cardiovascular Disease ◽

Cardiovascular Diseases ◽

Trace Element ◽

Ischemia Reperfusion ◽

Myocardial Damage ◽

Selenium Deficiency ◽

Coronary Syndrome ◽

Increased Risk ◽

Postinfarction Remodeling

THE ROLE OF TRACE ELEMENT SELENIUM IN CARDIOVASCULAR DISEASE DEVELOPMENT (review) Zhuravlyova L.V., Filonenko M.V. Balanced levels of trace element selenium are of high importance for many of the body’s regulatory and metabolic functions. Reduction in selenium supply in humans can lead to an increased risk of various pathologies, including cardiovascular diseases. This article considers the contemporary opinions on the role of selenium in physiology and pathophysiology of the cardiovascular system. A particular attention is payed to the effects of selenium deficiency on the development of acute coronary syndrome, including myocardial damage after ischemia/reperfusion and postinfarction remodeling of the left ventricle. Also, the intrinsic properties of selenium for inhibition of apoptosis are highlighted. Keywords: selenium, selenoproteins, cardiovascular disease. Резюме РОЛЬ МІКРОЕЛЕМЕНТУ СЕЛЕНУ В РОЗВИТКУ СЕРЦЕВО-СУДИННИХ ЗАХВОРЮВАНЬ Журавльова Л.В., Філоненко М.В. Збалансовані рівні мікроелементу селену мають велике значення для багатьох регуляторних та метаболічних функцій організму. Зниження надходження селену в організм людини може призвести до підвищеного ризику розвитку різних патологій, включаючи серцево-судинні захворювання. В статті розглянуто сучасні погляди на роль селену в забезпеченні функціонування серцево-судинної системи. Особливої уваги приділено впливу дефіциту селену на розвиток гострого коронарного синдрому, включаючи ураження міокарда після ішемії / реперфузії та постінфарктного ремоделювання лівого шлуночка. Також виствітлено аспекти внутрішніх властивостей селену щодо інгібування апоптозу. Ключові слова: селен, селенопротеїни, серцево-судинні захворювання. Резюме РОЛЬ МИКРОЭЛЕМЕНТА СЕЛЕНА В РАЗВИТИИ СЕРДЕЧНО-СОСУДИСТЫХ ЗАБОЛЕВАНИЙ Журавлева Л.В., Филоненко М.В. Сбалансированный уровень микроэлемента селена имеет большое значение для многих регуляторных и метаболических функций организма. Снижение поступления селена в организм может привести к увеличению риска развития различных патологий, в том числе сердечно-сосудистых заболеваний. В данной статье рассмотрены современные взгляды на роль селена в обеспечении функционирования сердечно-сосудистой системы. Особое внимание уделено влиянию дефицита селена на развитие острого коронарного синдрома, включая повреждение миокарда после ишемии / реперфузии и постинфарктного ремоделирования левого желудочка. Также освещены аспекты внутренних свойств селена по ингибированию апоптоза. Ключевые слова: селен, селенопротеины, сердечно-сосудистые заболевания.

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MicroRNAs in Noise-Induced Hearing Loss and their Regulation by Oxidative Stress and Inflammation

Current Drug Targets ◽

10.2174/1389450121666200615145552 ◽

2020 ◽

Vol 21 (12) ◽

pp. 1216-1224

Author(s):

Fatemeh Forouzanfar ◽

Samira Asgharzade

Keyword(s):

Oxidative Stress ◽

Hearing Loss ◽

Hair Cell ◽

Noise Exposure ◽

Cell Damage ◽

Sensory Cells ◽

Noise Induced Hearing Loss ◽

Irreversible Damage ◽

Open Access Journals

Noise exposure (NE) has been recognized as one of the causes of sensorineural hearing loss (SNHL), which can bring about irreversible damage to sensory hair cells in the cochlea, through the launch of oxidative stress pathways and inflammation. Accordingly, determining the molecular mechanism involved in regulating hair cell apoptosis via NE is essential to prevent hair cell damage. However, the role of microRNAs (miRNAs) in the degeneration of sensory cells of the cochlea during NE has not been so far uncovered. Thus, the main purpose of this study was to demonstrate the regulatory role of miRNAs in the oxidative stress pathway and inflammation induced by NE. In this respect, articles related to noise-induced hearing loss (NIHL), oxidative stress, inflammation, and miRNA from various databases of Directory of Open Access Journals (DOAJ), Google Scholar, PubMed; Library, Information Science & Technology Abstracts (LISTA), and Web of Science were searched and retrieved. The findings revealed that several studies had suggested that up-regulation of miR-1229-5p, miR-451a, 185-5p, 186 and down-regulation of miRNA-96/182/183 and miR-30b were involved in oxidative stress and inflammation which could be used as biomarkers for NIHL. There was also a close relationship between NIHL and miRNAs, but further research is required to prove a causal association between miRNA alterations and NE, and also to determine miRNAs as biomarkers indicating responses to NE.

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Regulation of miRNAs by Natural Antioxidants in Cardiovascular Diseases: Focus on SIRT1 and eNOS

Antioxidants ◽

10.3390/antiox10030377 ◽

2021 ◽

Vol 10 (3) ◽

pp. 377

Author(s):

Yunna Lee ◽

Eunok Im

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Endothelial Dysfunction ◽

Natural Antioxidants ◽

Sirtuin 1 ◽

Potential Benefits ◽

New Perspective ◽

Oxide Synthase ◽

Endothelial Nitric Oxide

Cardiovascular diseases (CVDs) are the most common cause of morbidity and mortality worldwide. The potential benefits of natural antioxidants derived from supplemental nutrients against CVDs are well known. Remarkably, natural antioxidants exert cardioprotective effects by reducing oxidative stress, increasing vasodilation, and normalizing endothelial dysfunction. Recently, considerable evidence has highlighted an important role played by the synergistic interaction between endothelial nitric oxide synthase (eNOS) and sirtuin 1 (SIRT1) in the maintenance of endothelial function. To provide a new perspective on the role of natural antioxidants against CVDs, we focused on microRNAs (miRNAs), which are important posttranscriptional modulators in human diseases. Several miRNAs are regulated via the consumption of natural antioxidants and are related to the regulation of oxidative stress by targeting eNOS and/or SIRT1. In this review, we have discussed the specific molecular regulation of eNOS/SIRT1-related endothelial dysfunction and its contribution to CVD pathologies; furthermore, we selected nine different miRNAs that target the expression of eNOS and SIRT1 in CVDs. Additionally, we have summarized the alteration of miRNA expression and regulation of activities of miRNA through natural antioxidant consumption.

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Glutathione Participation in the Prevention of Cardiovascular Diseases

Antioxidants ◽

10.3390/antiox10081220 ◽

2021 ◽

Vol 10 (8) ◽

pp. 1220

Author(s):

Deyamira Matuz-Mares ◽

Héctor Riveros-Rosas ◽

María Magdalena Vilchis-Landeros ◽

Héctor Vázquez-Meza

Keyword(s):

Cardiovascular Diseases ◽

Superoxide Anion ◽

Reactive Nitrogen Species ◽

Hypochlorous Acid ◽

Reduced Glutathione ◽

Heart Diseases ◽

Reactive Species ◽

Oxygen Species ◽

Cardiovascular Pathologies

Cardiovascular diseases (CVD) (such as occlusion of the coronary arteries, hypertensive heart diseases and strokes) are diseases that generate thousands of patients with a high mortality rate worldwide. Many of these cardiovascular pathologies, during their development, generate a state of oxidative stress that leads to a deterioration in the patient’s conditions associated with the generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). Within these reactive species we find superoxide anion (O2•–), hydroxyl radical (•OH), nitric oxide (NO•), as well as other species of non-free radicals such as hydrogen peroxide (H2O2), hypochlorous acid (HClO) and peroxynitrite (ONOO–). A molecule that actively participates in counteracting the oxidizing effect of reactive species is reduced glutathione (GSH), a tripeptide that is present in all tissues and that its synthesis and/or regeneration is very important to be able to respond to the increase in oxidizing agents. In this review, we will address the role of glutathione, its synthesis in both the heart and the liver, and its importance in preventing or reducing deleterious ROS effects in cardiovascular diseases.

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DDAH gene and cardiovascular risk

Vascular Medicine ◽

10.1177/1358836x0501000107 ◽

2005 ◽

Vol 10 (1_suppl) ◽

pp. S45-S48 ◽

Cited By ~ 29

Author(s):

Veli-Pekka Valkonen ◽

Tomi-Pekka Tuomainen ◽

Reijo Laaksonen

Keyword(s):

Cardiovascular Risk ◽

Cardiovascular Diseases ◽

High Plasma ◽

No Synthase ◽

Clinical Role ◽

Plasma Adma ◽

Increased Risk ◽

Major Route ◽

Increased Susceptibility

The crucial role of nitric oxide (NO) for normal endothelial function is well known. In many conditions associated with increased risk of cardiovascular diseases such as hypercholesterolemia, hypertension, abdominal obesity, diabetes and smok ing, NO biosynthesis is dysregulated, leading to endothelial dysfunction. The grow ing evidence from animal and human studies indicates that endogenous inhibitors of endothelial NO synthase such as asymmetric dimethylarginine (ADMA) and NG-monomethyl-L-arginine (L-NMMA) are associated with the endothelial dysfunc tion and potentially regulate NO synthase. The major route of elimination of ADMA is metabolism by the enzymes dimethylarginine dimethylaminohydrolase-1 and -2 (DDAH). In our recent study 16 men with either low or high plasma ADMA concen trations were screened to identify DDAH polymorphisms that could potentially be associated with increased susceptibility to cardiovascular diseases. In that study a novel functional mutation of DDAH-1 was identified; the mutation carriers had a significantly elevated risk for cardiovascular disease and a tendency to develop hypertension. These results confirmed the clinical role of DDAH enzymes in ADMA metabolism. Furthermore, it is possible that more common variants of DDAH genes contribute more widely to increased cardiovascular risk.

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PHYSICAL ACTIVITY AS HEALTHY INTERVENTION AGAINST SEVERE OXIDATIVE STRESS IN ELDERLY POPULATION

Journal of Frailty & Aging ◽

10.14283/jfa.2013.20 ◽

2013 ◽

pp. 1-9

Author(s):

C. TOMAS-ZAPICO ◽

E. IGLESIAS-GUTIERREZ ◽

B. FERNANDEZ-GARCIA ◽

D. DE GONZALO-CALVO

Keyword(s):

Oxidative Stress ◽

Physical Activity ◽

Elderly Population ◽

Physiological Basis ◽

Related Disease ◽

Age Related ◽

Wide Range ◽

Health Related ◽

Relevant Risk Factor

Severe oxidative stress is a relevant risk factor for major deleterious health-related events in olderpeople and is thought to be an important contributor to age-related disease. Literature has suggested oxidativestress as a therapeutic target for mitigating the biological decline and attenuating the occurrence of adverseclinical events in aged individuals. However, definitive treatments are not known. Regular and moderate physicalactivity has been proposed as possible intervention for slowing age-related decline. This healthy strategy presentsa wide range of beneficial aspects for elderly, from the reduction of morbidity, disability, frailty and mortalityrates to treatment of many age-related disorders. Importantly, the global benefits on health are not shared by anyother strategies. Nevertheless, the physiological basis by which exercise produces its benefits to the organism isnot fully understood. This review summarizes the evidence for the role of physical activity as potential healthyintervention for mitigating the negative aspects of aging through the modulation of the oxidative mechanisms.

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Circulating Leukocytes and Oxidative Stress in Cardiovascular Diseases: A State of the Art

Oxidative Medicine and Cellular Longevity ◽

10.1155/2019/2650429 ◽

2019 ◽

Vol 2019 ◽

pp. 1-9 ◽

Cited By ~ 3

Author(s):

Speranza Rubattu ◽

Maurizio Forte ◽

Salvatore Raffa

Keyword(s):

Oxidative Stress ◽

Cardiovascular Diseases ◽

Stress Level ◽

Mononuclear Cells ◽

Pathological Condition ◽

Clinical Manifestations ◽

Therapeutic Interventions ◽

Oxidative Stress Level ◽

The Impact

Increased oxidative stress from both mitochondrial and cytosolic sources contributes to the development and the progression of cardiovascular diseases (CVDs), and it is a target of therapeutic interventions. The numerous efforts made over the last decades in order to develop tools able to monitor the oxidative stress level in patients affected by CVDs rely on the need to gain information on the disease state. However, this goal has not been satisfactorily accomplished until now. Among others, the isolation of circulating leukocytes to measure their oxidant level offers a valid, noninvasive challenge that has been tested in few pathological contexts, including hypertension, atherosclerosis and its clinical manifestations, and heart failure. Since leukocytes circulate in the blood stream, it is expected that they might reflect quite closely both systemic and cardiovascular oxidative stress and provide useful information on the pathological condition. The results of the studies discussed in the present review article are promising. They highlight the importance of measuring oxidative stress level in circulating mononuclear cells in different CVDs with a consistent correlation between degree of oxidative stress and severity of CVD and of its complications. Importantly, they also point to a double role of leukocytes, both as a marker of disease condition and as a direct contributor to disease progression. Finally, they show that the oxidative stress level of leukocytes reflects the impact of therapeutic interventions. It is likely that the isolation of leukocytes and the measurement of oxidative stress, once adequately developed, may represent an eligible tool for both research and clinical purposes to monitor the role of oxidative stress on the promotion and progression of CVDs, as well as the impact of therapies.

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