Redox Experimental Medicine最新文献_第3页

Redox Experimental Medicine: Linking redox research to human health and disease 氧化还原实验医学:将氧化还原研究与人类健康和疾病联系起来

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0014

G. Poli

引用次数: 0

Circulating Oxysterols in Alzheimer’s disease: A Systematic Review and Meta-analysis 阿尔茨海默病的循环氧甾醇:一项系统综述和荟萃分析

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0009

O. S. Ademowo, I. Dias

{"title":"Circulating Oxysterols in Alzheimer’s disease: A Systematic Review and Meta-analysis","authors":"O. S. Ademowo, I. Dias","doi":"10.1530/rem-22-0009","DOIUrl":"https://doi.org/10.1530/rem-22-0009","url":null,"abstract":"Despite decades of research, the cause and series of events underlying the advancement of Alzheimer’s disease (AD) has not yet been established. Lipids and especially cholesterol levels have been proposed to be implicated in AD. Several studies have been undertaken and many ongoing in different directions looking at the importance of circulating cholesterols and oxidised cholesterols in Alzheimer’s disease with inconsistent methods and results. This meta-analysis aims to systematically analyse available data describing the involvement of oxidised cholesterols in Mild cognitive impairment (MCI) and Alzheimer’s disease (AD). We conducted a systematic literature search of 6 databases MEDLINE (PubMed), BIOSIS (Web of Science), EMBASE (Elsevier), PsycNET, Scopus and Cochrane library for studies measuring oxysterols (24-hydroxycholesterol (24OHC); 26-hydroxycholesterol (26OHC) and 7-oxycholesterols) in serum or plasma from MCI / AD patients compared to age and gender matched cognitively normal controls. Data was analysed using the inverse variance and standard mean difference with random effect analysis model at 95% confidence interval for association between oxysterols and MCI / AD in Review Manager (RevMan) software version 5.4.1. 175 studies between January 2000 and April 2022 were identified by 2 independent researchers out of which 14 met the inclusion criteria and were analysed with a total of 957 controls, 469 MCI cases and 509 AD cases. The standard mean differences between MCI / AD participants and controls did not show any difference in the oxysterol levels except for 26OHC level which were higher in AD but not statistically significant.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"87 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126190518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

High cholesterol diet, oxysterols and their impact on the gut–brain axis 高胆固醇饮食、氧化甾醇及其对肠脑轴的影响

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0003

G. Poli, Noemi Iaia, Valerio Leoni, F. Biasi

{"title":"High cholesterol diet, oxysterols and their impact on the gut–brain axis","authors":"G. Poli, Noemi Iaia, Valerio Leoni, F. Biasi","doi":"10.1530/rem-22-0003","DOIUrl":"https://doi.org/10.1530/rem-22-0003","url":null,"abstract":"In a Western or Westernized diet, the abundant cholesterol is invariably associated with the presence of biochemically reactive oxysterols, the amount of which mainly depends upon the autoxidation degree of cholesterol itself, during food harvesting, production and storage. Oxysterols, in the average amount and composition detected in a high-cholesterol diet, display remarkable pro-inflammatory and cytotoxic effects on the gut epithelium. Moreover, in a low micromolar range, they may change the physiological level and membrane localization of tight junctions of the intestinal epithelial barrier, which then become leaky and permeable to microbiota. This combination of toxic effects possibly exerted by dietary oxysterols likely contributes to the impairment of the microbiota–gut–brain axis, through both direct and indirect mechanisms hereby reviewed. Importantly, dietary oxysterols are absorbed like cholesterol and circulate in the bloodstream, mainly within LDLs, rendering these micelles more oxidized and dangerous. Last but not the least, dietary oxysterols may deeply interfere with correct gut–brain signalling because of the redox pathways they are hyper-regulating and sustaining. In conclusion, protective dietary measures should be adopted, including restricted consumption of cholesterol-rich food and reduction of cholesterol autoxidation in food production and storage, for instance by supplementation of food with flavonoids and/or other bioactive substances with strong anti-oxysterol properties.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131228107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4

Sirtuins as potential therapeutic targets for mitigating OxInflammation in typical Rett syndrome: plausible mechanisms and evidence Sirtuins作为减轻典型Rett综合征氧化炎症的潜在治疗靶点:合理的机制和证据

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0004

Valeria Cordone, A. Pecorelli, G. Valacchi

{"title":"Sirtuins as potential therapeutic targets for mitigating OxInflammation in typical Rett syndrome: plausible mechanisms and evidence","authors":"Valeria Cordone, A. Pecorelli, G. Valacchi","doi":"10.1530/rem-22-0004","DOIUrl":"https://doi.org/10.1530/rem-22-0004","url":null,"abstract":"\u0000\u0000\u0000\u0000\u0000\u0000Rett 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.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"62 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"123459707","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Sources of 7-ketocholesterol, metabolism and inactivation strategies: food and biomedical applications 7-酮胆固醇的来源、代谢和失活策略:食品和生物医学应用

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0005

I. Ghzaiel, K. Sassi, A. Zarrouk, Shubhrima Ghosh, I. Dias, T. Nury, Mohamed Ksila, Soukaina Essadek, Mounia Tahri Joutey, F. Brahmi, Wafa Mihoubi, S. Rup-Jacques, M. Samadi, L. Rezig, S. Meziane, Taoufik Ghrairi, Olfa Masmoudi-Kouki, S. Hammami, B. Nasser, M. Hammami, Yuqin Wang, W. Griffiths, A. Vejux, G. Lizard

{"title":"Sources of 7-ketocholesterol, metabolism and inactivation strategies: food and biomedical applications","authors":"I. Ghzaiel, K. Sassi, A. Zarrouk, Shubhrima Ghosh, I. Dias, T. Nury, Mohamed Ksila, Soukaina Essadek, Mounia Tahri Joutey, F. Brahmi, Wafa Mihoubi, S. Rup-Jacques, M. Samadi, L. Rezig, S. Meziane, Taoufik Ghrairi, Olfa Masmoudi-Kouki, S. Hammami, B. Nasser, M. Hammami, Yuqin Wang, W. Griffiths, A. Vejux, G. Lizard","doi":"10.1530/rem-22-0005","DOIUrl":"https://doi.org/10.1530/rem-22-0005","url":null,"abstract":"\u0000\u0000\u0000\u0000\u0000\u00007-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.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"32 16","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"120994343","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 7

Oxidative stress in nonalcoholic fatty liver disease: a reappraisal of the role in supporting inflammatory mechanisms 氧化应激在非酒精性脂肪性肝病中的作用:支持炎症机制的重新评估

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0002

S. Sutti, E. Albano

引用次数: 1

Potential benefits of nutritional supplementation in diabetic sarcopenia 营养补充对糖尿病肌少症的潜在益处

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0001

Heaji Lee, S. Yang, Y. Lim

引用次数: 3

Essential trace element selenium and redox regulation-its metabolism, physiological function, and related diseases 必需微量元素硒及其氧化还原调控——代谢、生理功能及相关疾病

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0010

Yoshiro Saito

{"title":"Essential trace element selenium and redox regulation-its metabolism, physiological function, and related diseases","authors":"Yoshiro Saito","doi":"10.1530/rem-22-0010","DOIUrl":"https://doi.org/10.1530/rem-22-0010","url":null,"abstract":"The essential trace element selenium plays a significant role in redox homeostasis in the human body. Selenium is very reactive and has a potent toxicity; however, the living body cleverly utilizes its reactivity for redox reactions. The biological function of selenium is mainly mediated by selenoproteins, which contain selenocysteine, a cysteine analogue that possesses selenium instead of sulphur. Twenty-five types of human selenoproteins have been identified, including glutathione peroxidase (GPX; for the reduction of hydrogen peroxide and lipid hydroperoxide) and thioredoxin reductase (for redox regulation). Selenoprotein P (SELENOP), which is a major selenoprotein in the plasma, is mainly synthesized in the liver and secreted into the plasma. As a multifunctional protein with selenium-transport activity, GPX-like activity and metal-binding properties, SELENOP plays a vital role in selenium metabolism and redox regulation. This review focuses on the relationship between selenium metabolism and redox regulation, particularly the physiological role of selenoproteins and the pathophysiological implications of its disorder. Furthermore, the significant roles of selenium in infectious diseases and its utility for phylaxis are discussed.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"26 2","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"114130467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Post-translational modifications of endothelial nitric oxide synthase induced by oxidative stress in vascular diseases 血管疾病中氧化应激诱导内皮一氧化氮合酶的翻译后修饰

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0013

A. Nègre-Salvayre, A. Swiader, P. Guerby, R. Salvayre

{"title":"Post-translational modifications of endothelial nitric oxide synthase induced by oxidative stress in vascular diseases","authors":"A. Nègre-Salvayre, A. Swiader, P. Guerby, R. Salvayre","doi":"10.1530/rem-22-0013","DOIUrl":"https://doi.org/10.1530/rem-22-0013","url":null,"abstract":"Endothelial nitric oxide 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, nitric oxide is synthesized by the endothelial nitric oxide synthase which is activated by dimerization in the presence of L-arginine (as substrate) and several cofactors including the essential cofactor tetrahydrobiopterin. The nitric oxide/endothelial nitric oxide synthase pathway is basically vasculoprotective and antiatherogenic but it may become dysfunctional and proatherogenic under conditions which locally increase the production of reactive oxygen species, leading to tetrahydrobiopterin oxidation, endothelial nitric oxide synthase dysfunction and uncoupling. In these conditions, endothelial nitric oxide synthase switches from a nitric oxide-producing to superoxide anion-producing enzyme, which potentiates oxidative and nitrosative stress via the generation of peroxynitrite. In redox-perturbed conditions, endothelial nitric oxide synthase 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 endothelial nitric oxide synthase by lipid-oxidation derived aldehydes or from hyperglycemia-induced modifications. In this review, we summarize the mechanisms by which these post-translational modifications alter endothelial nitric oxide synthase activity, and their potential implication in the pathophysiology of vascular diseases.\u0000","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"182 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"126775696","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Redox experimental medicine and liver regeneration 氧化还原实验医学与肝脏再生

Redox Experimental Medicine Pub Date : 2022-07-01 DOI: 10.1530/rem-22-0008

F. Bellanti, G. Vendemiale, G. Serviddio

{"title":"Redox experimental medicine and liver regeneration","authors":"F. Bellanti, G. Vendemiale, G. Serviddio","doi":"10.1530/rem-22-0008","DOIUrl":"https://doi.org/10.1530/rem-22-0008","url":null,"abstract":"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.\u0000Several 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.","PeriodicalId":310409,"journal":{"name":"Redox Experimental Medicine","volume":"7 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"127551950","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2