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Endothelial nitric oxide (NO) plays a critical role in vascular homeostasis. It regulates the vascular tone, maintains the blood flow, exerts a vasorelaxing effect on smooth muscle cells and inhibits their proliferation. In the endothelium, NO is synthesized by the endothelial NO synthase which is activated by dimerization in the presence of l-arginine (as substrate) and several cofactors including the essential cofactor tetrahydrobiopterin. The NO/eNOS pathway is basically vasculoprotective and antiatherogenic but it may become dysfunctional and proatherogenic under conditions that locally increase the production of reactive oxygen species, leading to tetrahydrobiopterin oxidation, eNOS dysfunction and uncoupling. In these conditions, eNO synthase switches from a NO-producing to superoxide anion-producing enzyme, which potentiates oxidative and nitrosative stress via the generation of peroxynitrite. In redox-perturbed conditions, eNOS dysfunction may also result from post-translational modifications deriving from oxidative stress such as S-glutathionylation or resulting either from the formation of adducts on eNOS by lipid-oxidation-derived aldehydes or from hyperglycemia-induced modifications. In this review, we summarize the mechanisms by which these post-translational modifications alter eNOS activity, and their potential implication in the pathophysiology of vascular diseases.
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Type 2 diabetes mellitus, one of the metabolic diseases, is a major risk factor for impaired muscle function leading to muscle loss, weakness, and frailty. A lot of studies have suggested that the biological mechanisms which contribute to diabetic sarcopenia, including insulin resistance, altered energy metabolism, oxidative stress, and inflammation. Although different nutritional interventions for diabetic sarcopenia have not been clearly defined, there is no doubt that nutrition plays an essential role in the prevention or delay of muscle loss and maintenance of physical function. In this review, we discuss the recent literature on biological pathways for diabetic sarcopenia and potent nutrients used for attenuating diabetic sarcopenia: dietary proteins, omega-3 fatty acids, vitamin D, vitamin E, and other anti-oxidants for future research.
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The liver is characterized by unique regenerative properties to restore its mass and function after a partial loss. Hepatic regeneration arises after resection or following acute and chronic injuries. Resection and acute liver damage normally induce a regenerative process characterized by phenotypic fidelity, in which each cell type promotes its own replication and replacement. This process fails in chronic liver damage, where trans-differentiation of parenchymal cells or activation of facultative progenitors occurs. Both liver resection and acute/chronic damages alter redox homeostasis, as a consequence of blood flow changes, hypoxia, metabolism modification, and activation of inflammatory response. Even though formerly described as ‘oxidative stress’, altered redox homeostasis leads to the fine regulation of several pathways involved in liver regeneration, including the proliferation of parenchymal cells, trans-differentiation, and activation of facultative progenitors.
Several redox-dependent transcription factors and pathways implicated in the regenerative process of the liver were described, but pre-clinical experiments using different antioxidants were not fully conclusive. Even though accurate study designs to define appropriate dosages, treatment duration, and routes of administration are required, modulation of redox-dependent molecular pathways to enhance liver regeneration is even more intriguing. Preliminary studies focused on the identification of these targets will pave the way for viable therapies to be tested in clinical trials.
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Despite the great progress and advancements in scientific knowledge, technology, and medicine, viral infections continue to put human health in trouble. Both acquired immunodeficiency syndrome (AIDS) and coronavirus disease 2019 (COVID-19), caused by human immunodeficiency virus and severe acute respiratory syndrome coronavirus 2, two RNA viruses responsible for global pandemics, respectively, have poor outcomes associated with increased oxidative stress, systemic inflammation, and immunopathology. Here, we have collected the current knowledge linking both viral infections, focusing on the role of oxidative stress and the redox balance. Furthermore, we provide information on some redox-active compounds, such as vitamins, thiol-based agents, and polyphenols, and their possible beneficial effects on both diseases. Thus, in this review, we aim to highlight the importance and impact of nutritional strategies to strengthen our immune system, especially to increase the effectiveness of pharmacological treatments, or when there are no effective treatments.
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The highly conserved DJ-1 protein fundamentally acts as a redox sensor conferring antioxidative cytoprotection under oxidative insults. DJ-1 preferentially undergoes oxidation at 106 cysteine residue (C106) under oxidative stress. Although initially identified as an oncogene, emerging evidence suggests the essential roles of DJ-1 in modulating numerous physiological processes involved in cellular growth, development, survival, and death. Compromised DJ-1 expression and function directly or indirectly trigger signaling cascades leading to pathophysiological conditions including neurodegeneration, cancer, stroke, and inflammatory diseases. Besides the intracellular functions, enhanced DJ-1 secretion into the extracellular fluid, including cerebrospinal fluid and blood, is related to Parkinson’s disease (PD) and cancer pathogenesis. Here, we review the current knowledge regarding DJ-1’s roles as a ubiquitous cytoprotective protein controlling numerous signaling pathways, secretion, and therapeutic potentials.
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Animal Science Department, Plants for Human Health Institute, North Carolina State University, Kannapolis Research Campus, Kannapolis, North Carolina, USA
Department of Food and Nutrition, Kyung Hee University, Seoul, South Korea
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Rett syndrome (RTT), a monogenic neurodevelopmental disorder mainly affecting female, is caused by mutations in X-linked MECP2 gene, an ubiquitous epigenetic regulator. In addition to neurological issues, RTT patients show a variety of multisystem manifestations and impairment of different signalling and metabolic pathways, including compromised mitochondrial function, altered redox homeostasis, improper cholesterol metabolism and subclinical inflammation. The sirtuin family (SIRTs), comprising seven members, catalyses the NAD+-dependent deacetylation, ADP-ribosylation and deacylation of a wide range of targets and works as sensors of cellular energetic status. In addition, SIRTs can modulate activities and gene expression of proteins involved in cellular stress responses related to oxidative stress, mitochondrial dysfunctions and inflammation, in both physiological and pathological conditions. Given some shared molecular aspects, herein, we revised the current scientific literature and hypothesized the possible relationship of SIRTs signalling involvement in RTT pathogenesis and OxInflammation. Although further research is needed, uncovering the possible involvement of SIRTs in RTT could reveal new potential pharmacological targets for the disorder. In light of this, SIRT-enhancing compounds could likely represent a new option to be tested as co-adjuvant alternatives to the current therapies.
Lab-NAFS ‘Nutrition-Functional Food & Vascular Health’, Faculty of Medicine, University of Monastir, Monastir, Tunisia
Faculty of Sciences of Tunis, University Tunis-El Manar, Tunis, Tunisia
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Faculty of Medicine, University of Sousse, Sousse, Tunisia
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Department of Biology, Faculty of Sciences, University Tunis-El Manar, Loboratory of Neurophysiology, Cellular Physiopathology and Valorisation of BioMolecules, LR18ES03, Tunis, Tunisia
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Laboratory of Biochemistry, Neurosciences, Natural Resources and Environment, Faculty of Sciences & Techniques, University Hassan I, Settat, Morocco
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Laboratory of Biochemistry, Neurosciences, Natural Resources and Environment, Faculty of Sciences & Techniques, University Hassan I, Settat, Morocco
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University of Carthage, High Institute of Food Industries, El Khadra City, Tunis, Tunisia
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Graphical abstract
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7-Ketocholesterol (or 7-oxocholesterol) is an oxysterol essentially formed by cholesterol autoxidation. It is often found at enhanced levels in the body fluids and/or target tissues of patients with age-related diseases (cardiovascular, neuronal, and ocular diseases) as well as in subjects concerned with civilization diseases (type 2 diabetes, bowel diseases, and metabolic syndrome). The involvement of increased 7-ketocholesterol levels in the pathophysiology of these diseases is widely suspected. Indeed, 7-ketocholesterol at elevated concentrations is a powerful inducer of oxidative stress, inflammation, and cellular degeneration which are common features of all these diseases. It is important to better know the origin of 7-ketocholesterol (diet, incidence of environmental factors, and endogenous formation (autoxidation and enzymatic synthesis)) and its inactivation mechanisms which include esterification, sulfation, oxidation, and reduction. This knowledge will make it possible to act at different levels to regulate 7-ketocholesterol level and counteract its toxicity in order to limit the incidence of diseases associated with this oxysterol. These different points as well as food and biomedical applications are addressed in this review.
Search for other papers by Aranzazu M de Marañón in
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Department of Physiology, University of Valencia, Valencia, Spain
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CIBERehd – Department of Pharmacology, University of Valencia, Valencia, Spain
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Department of Physiology, University of Valencia, Valencia, Spain
CIBERehd – Department of Pharmacology, University of Valencia, Valencia, Spain
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Type 2 diabetes is a chronic metabolic disease characterized by the development of low-grade systemic inflammation, hyperglycaemia, and hyperlipidaemia. These pathogenic traits have a profound impact on mitochondrial function as mitochondria serve as intermediary organelles between nutrients and energy production. Moreover, the mitochondrial quality control system is also altered and rendered defective by type 2 diabetes. These alterations entail the accumulation of defective mitochondria, which causes the diabetic background to deteriorate further. In this context, it is of paramount importance to improve mitochondrial function and ameliorate the consequences of mitochondrial dysfunction. This review assesses different treatments that target mitochondrial dysfunction as a way of treating type 2 diabetes. Lifestyle interventions and pharmacological treatments such as biguanides, thiazolidinediones, a-glucosidase inhibitors, glucagon-like peptide 1 receptor agonists, or sodium-glucose co-transporter-2 inhibitors protect mitochondrial function, while novel mitochondria-targeted molecules including natural compounds, mitochondria-targeted antioxidants, inhibitors of mitochondria pore transition pore opening, NO and H2S donors, and inhibitors of mitochondrial fission positively impact on mitochondrial function and its quality control mechanisms. Most of these therapeutic tools require more research, but they already show promising therapeutic mechanisms that improve type 2 diabetes and its cellular consequences.
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Redox Experimental Medicine is a new, fully open-access, peer-reviewed journal publishing redox research that advances our understanding of the effect of redox processes on human health and disease.
Aberrations in redox processes can have a profound impact on the normal physiology of humans, with implications in many diseases. Redox Experimental Medicine will serve as an essential publication for the international scientific community to translate experimental knowledge to redox-based preventive and/or therapeutic interventions, with a view to advancing health. The journal will publish basic and translational articles which have potential therapeutic relevance, as well as pre-clinical and clinical studies.
Led by Editor-in-Chief Professor Giuseppe Poli, from the University of Turin, Redox Experimental Medicine’s highly accomplished and internationally diverse Editorial Board will oversee the rigorous yet rapid peer review of articles.
In his launch Editorial, Professor Poli explains how the journal focuses on an underserved area, commenting that "the experimental investigation of the pathophysiological role of a single molecule or a molecular pathway is certainly essential, but it cannot stand alone and needs to be part of a more comprehensive study project, taking into account the complex reality of the human organism".
Bioscientifica is sponsoring the article publication charge until the end of 2023, enabling Redox Experimental Medicine authors to publish their research on an open-access basis free of charge, offering greater reach and visibility of their work.
Redox Experimental Medicine is now open for submissions. Please take a look at the scope for a full list of topics covered by the journal.
About Bioscientifica
Bioscientifica exists to support biomedicine. Through our publishing expertise we strengthen biomedical communities to advance science and health. Bioscientifica is owned by the UK’s Society for Endocrinology and any profits made through our publications are redistributed to support biomedical research and practice.
