Oxidative Stress and New Pathogenetic Mechanisms in Endothelial Dysfunction: Potential Diagnostic Biomarkers and Therapeutic Targets

Scioli, Maria Giovanna; Storti, Gabriele; D’Amico, Federico; Guzmán, Roger Rodríguez; Centofanti, Federica; Doldo, Elena; Miranda, Ela María Céspedes; Orlandi, Augusto

doi:10.3390/jcm9061995

Cited by 112 publications

(78 citation statements)

References 306 publications

(393 reference statements)

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“…Endothelial dysfunction, including hypertension and atherosclerosis, is the main risk factor for stroke, myocardial infarction, and heart failure. Endothelial dysfunction is defined as a decreased production and availability of NO, with or without an imbalance between endothelium-derived contracting and relaxing factors associated with a pro-inflammatory and prothrombotic status [46]. Under oxidative stress, ROS are able to mediate endothelial dysfunction and vascular abnormalities by disrupting the vasoprotective NO signaling pathway, leading to NO synthase (NOS) uncoupling.…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

“…Finally, numerous randomized studies are currently in progress to evaluate the effects of dietary supplementation with mitoquinone in several conditions, including diastolic dysfunction (NCT03586414), peripheral arterial disease (NCT03506633), or chronic kidney disease (NCT02364648) [46], but the impact of mitoquinone supplementation in patients remains to be determined.…”

Section: Clinical Trialsmentioning

confidence: 99%

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Oxidative Stress in Cardiovascular Diseases

et al. 2020

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Reactive oxygen species (ROS) are subcellular messengers in signal transductions pathways with both beneficial and deleterious roles. ROS are generated as a by-product of mitochondrial respiration or metabolism or by specific enzymes such as superoxide dismutases, glutathione peroxidase, catalase, peroxiredoxins, and myeloperoxidases. Under physiological conditions, the low levels of ROS production are equivalent to their detoxification, playing a major role in cellular signaling and function. In pathological situations, particularly atherosclerosis or hypertension, the release of ROS exceeds endogenous antioxidant capacity, leading to cell death. At cardiovascular levels, oxidative stress is highly implicated in myocardial infarction, ischemia/reperfusion, or heart failure. Here, we will first detail the physiological role of low ROS production in the heart and the vessels. Indeed, ROS are able to regulate multiple cardiovascular functions, such as cell proliferation, migration, and death. Second, we will investigate the implication of oxidative stress in cardiovascular diseases. Then, we will focus on ROS produced by NAPDH oxidase or during endothelial or mitochondrial dysfunction. Given the importance of oxidative stress at the cardiovascular level, antioxidant therapies could be a real benefit. In the last part of this review, we will detail the new therapeutic strategies potentially involved in cardiovascular protection and currently under study.

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Section: Endothelial Dysfunctionmentioning

confidence: 99%

Section: Clinical Trialsmentioning

confidence: 99%

Oxidative Stress in Cardiovascular Diseases

et al. 2020

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“…Under physiological conditions, ROS act as essential mediators of the redox signaling pathways involved in various cellular responses including proliferation, migration, differentiation or gene expression. In pathological situations, ROS is generated in excess, becoming toxic for cells, which leads to oxidation of molecules, enhancement of the inflammatory response, cellular aging or apoptosis [ 67 ]. Oxidative stress results from the imbalance between ROS production and ROS detoxification.…”

Section: Glycated Lipoproteins Detrimental Actions In Endothelial mentioning

confidence: 99%

Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies

2020

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Diabetes and its vascular complications affect an increasing number of people. This disease of epidemic proportion nowadays involves abnormalities of large and small blood vessels, all commencing with alterations of the endothelial cell (EC) functions. Cardiovascular diseases are a major cause of death and disability among diabetic patients. In diabetes, EC dysfunction (ECD) is induced by the pathological increase of glucose and by the appearance of advanced glycation end products (AGE) attached to the plasma proteins, including lipoproteins. AGE proteins interact with their specific receptors on EC plasma membrane promoting activation of signaling pathways, resulting in decreased nitric oxide bioavailability, increased intracellular oxidative and inflammatory stress, causing dysfunction and finally apoptosis of EC. Irreversibly glycated lipoproteins (AGE-Lp) were proven to have an important role in accelerating atherosclerosis in diabetes. The aim of the present review is to present up-to-date information connecting hyperglycemia, ECD and two classes of glycated Lp, glycated low-density lipoproteins and glycated high-density lipoproteins, which contribute to the aggravation of diabetes complications. We will highlight the role of dyslipidemia, oxidative and inflammatory stress and epigenetic risk factors, along with the specific mechanisms connecting them, as well as the new promising therapies to alleviate ECD in diabetes.

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“…Oxidative stress reflects an imbalance between the production of ROS and antioxidant defense systems. 74 It exerts an important role in the pathological process of malignant tumors, hypertension, diabetes, and even neurodegenerative diseases. [75][76][77] It is a conflict between antioxidant and oxidant balance, which results in cellular injury, and the imbalance may be caused by excessive ROS.…”

Section: Gstm3 In Ros and Oxidative Stressmentioning

confidence: 99%

<p>GSTM3 Function and Polymorphism in Cancer: Emerging but Promising</p>

Wang¹,

Yang²,

You³

et al. 2020

CMAR

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Cancer is a major cause of human mortality; however, the molecular mechanisms and proteomic biomarkers that cause tumor progression in malignant tumors are either unknown or only partially revealed. Glutathione S-transferases mu3 (GSTM3), which belongs to a family of xenobiotic detoxifying phase II enzymes, is associated with carcinogen detoxification and the metabolism of exogenous electrophilic substances. It has been reported that GSTM3 has different polymorphisms in various tumor cells and regulates tumorigenesis, cell invasion, metastasis, chemoresistance, and oxidative stress. Deep research into the regulatory mechanisms involved in disorders of GSTM3 expression and the function of GSTM3 in different cancers may facilitate improvements in cancer prevention and targeted therapy. The combination of GSTM3 with other family members can regulate the carcinogenesis and susceptibility to different cancers in humans. GSTM3 also regulates the reactive oxygen species (ROS) and participates in oxidative stress-mediated pathology. Here, we provide a general introduction to GSTM3 in order to better understand the role of GSTM3 in cancer.

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Oxidative Stress and New Pathogenetic Mechanisms in Endothelial Dysfunction: Potential Diagnostic Biomarkers and Therapeutic Targets

Cited by 112 publications

References 306 publications

Oxidative Stress in Cardiovascular Diseases

Oxidative Stress in Cardiovascular Diseases

Endothelial Dysfunction in Diabetes Is Aggravated by Glycated Lipoproteins; Novel Molecular Therapies

<p>GSTM3 Function and Polymorphism in Cancer: Emerging but Promising</p>

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