0000000000306465

AUTHOR

Antonio Cuadrado

showing 12 related works from this author

Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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Response to I. Batinic-Haberle et al.

2016

Letter to the editor.-- et al.

0301 basic medicinePhysiologybusiness.industryChemistryClinical BiochemistryCell Biologycomputer.software_genreBiochemistry03 medical and health sciences030104 developmental biologyComputingMethodologies_DOCUMENTANDTEXTPROCESSINGGeneral Earth and Planetary SciencesArtificial intelligencebusinessMolecular BiologycomputerNatural language processingGeneral Environmental ScienceAntioxidants & Redox Signaling
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Transcription factor NRF2 as a therapeutic target for chronic diseases: a systems medicine approach

2018

Systems medicine has a mechanism-based rather than a symptom- or organ-based approach to disease and identifies therapeutic targets in a nonhypothesis-driven manner. In this work, we apply this to transcription factor nuclear factor (erythroid-derived 2)-like 2 (NRF2) by cross-validating its position in a protein-protein interaction network (the NRF2 interactome) functionally linked to cytoprotection in low-grade stress, chronic inflammation, metabolic alterations, and reactive oxygen species formation. Multiscale network analysis of these molecular profiles suggests alterations of NRF2 expression and activity as a common mechanism in a subnetwork of diseases (the NRF2 diseasome). This netw…

0301 basic medicineRMSystems AnalysisNF-E2-Related Factor 2MedicinaNF-KAPPA-BAnti-Inflammatory AgentsTYPE-2 DIABETES-MELLITUSGENE PROMOTER POLYMORPHISMDiseaseComputational biologyInteractomeenvironment and public healthGLYCOGEN-SYNTHASE KINASETUMOR-SUPPRESSOR PTENNRF203 medical and health sciencesDrug DiscoveryAnimalsHumansTherapeutic targetsMedicineMolecular Targeted TherapyBardoxolone methylPLACEBO-CONTROLLED PHASE-3PharmacologyMechanism (biology)Drug discoverybusiness.industryDrug RepositioningRChronic inflammationrespiratory systemHEME OXYGENASE 1PROTEIN-PROTEIN INTERACTION3. Good healthSystems medicineDrug repositioning030104 developmental biologyDrug developmentEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISChronic DiseaseSystems medicineMolecular MedicineFUMARIC-ACID ESTERSbusiness
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High efficacy and safety of triple therapy in HCV genotype 1 and moderate fibrosis: a multicenter study of clinical practice in Spain.

2015

Background and rational. Telaprevir-based therapy (TBT) has been extensively evaluated in clinical trials. So we designed a study to compare the efficacy and safety of TBT between patients with moderate fibrosis and those suffering from advanced fibrosis in clinical practice. A multicenter observational and ambispective study was conducted. It included 582 patients with chronic hepatitis C genotype 1, 214 with fibrosis F2, and 368 with F3/F4 (F3: 148; F4: 220). Results. The mean patient age was 55 years, 67% male. Type of prior response was 22% naive, 57% relapsers, and 21% partial/null responders, 69% had high viral load (> 800,000 IU/mL). HCV genotypes were 1a (19%), 1b (69%), and 1 (12%)…

Liver CirrhosisMaleTime FactorsSpecialties of internal medicineHepacivirusGastroenterologySeverity of Illness IndexTelaprevirFibrosisRisk FactorsGenotypeGeneral MedicineMiddle AgedViral LoadTreatment OutcomeRC581-951Hepatitis C genotype 1RNA ViralDrug Therapy CombinationFemaleTelaprevir triple therapyModerate fibrosisViral loadOligopeptidesmedicine.drugAdultmedicine.medical_specialtyGenotypeAntiviral AgentsSafety and efficacyYoung AdultInternal medicinemedicineHumansAdverse effectAgedHepatologybusiness.industryInterleukinsHepatitis C Chronicmedicine.diseaseSurgeryDiscontinuationClinical trialSpainObservational studyInterferonsbusinessBiomarkersAnnals of hepatology
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Corrigendum to “European contribution to the study of ROS: A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS…

2018

The European Cooperation in Science and Technology (COST) provides an ideal framework to establish multi-disciplinary research networks. COST Action BM1203 (EU-ROS) represents a consortium of researchers from different disciplines who are dedicated to providing new insights and tools for better understanding redox biology and medicine and, in the long run, to finding new therapeutic strategies to target dysregulated redox processes in various diseases. This report highlights the major achievements of EU-ROS as well as research updates and new perspectives arising from its members. The EU-ROS consortium comprised more than 140 active members who worked together for four years on the topics b…

0301 basic medicineSocieties ScientificRedox signalingInternational CooperationClinical BiochemistryNanotechnologyReview ArticleBiologyPublic administrationBiochemistryAntioxidantsArticle03 medical and health sciencesmedia_common.cataloged_instanceAnimalsHumansCost actionEuropean UnionEuropean unionMolecular Biologylcsh:QH301-705.5media_commonFunding AgencyRedox therapeuticslcsh:R5-920Organic ChemistryReactive nitrogen species030104 developmental biologyWork (electrical)lcsh:Biology (General)Oxidative stressReactive Oxygen Specieslcsh:Medicine (General)Oxidation-ReductionSignal TransductionRedox Biology
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Antioxidants in Translational Medicine.

2015

This Open Access article is distributed under the terms of the Creative Commons Attribution Noncommercial License.-- et al.

GerontologyReactive oxygen species metabolismPhysiologyClinical BiochemistryComputingMilieux_LEGALASPECTSOFCOMPUTINGPharmacologyResveratrolmedicine.disease_causeBiochemistryAntioxidantschemistry.chemical_compoundNutraceuticalStilbenesMedicineAnimalsHumansMolecular BiologyTranslational Medical ResearchGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesbusiness.industryTranslational medicineOxidation reductionCell BiologyForum Review ArticlesOxidative StresschemistryClinical evidenceResveratrolGeneral Earth and Planetary SciencesbusinessReactive Oxygen SpeciesOxidation-ReductionOxidative stress
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Time-course of thiol oxidation of protein phosphatases during cerulein-induced acute pancreatitis

2018

Acute pancreatitis (AP) is an acute inflammatory process of the pancreatic gland. The aim of this work was to evaluate the role of thiol oxidation of key proteins that can be involved in the regulation of the inflammatory process during AP. AP was induced in C57BL/6 mice by 7 hourly subcutaneous injections of cerulein (50 ug/kg bw). Animals were sacrificed after 1, 3, 5 and 7 injections of cerulein. One hour after the first injection, hyperoxidation of peroxiredoxin 1–4 was detected coinciding with a H2O2 peak. Three hours later, a marked up-regulation of mRNA and protein expression of sulfiredoxin, partially mediated by Nrf-2, takes place. The up-regulation of sulfiredoxin seems to be resp…

0301 basic medicineMessenger RNA030102 biochemistry & molecular biologyChemistryp38 mitogen-activated protein kinasesThiol oxidationPhosphataseProtein phosphatase 2Pharmacologymedicine.diseaseBiochemistry03 medical and health sciencesSulfiredoxin0302 clinical medicine030220 oncology & carcinogenesisPhysiology (medical)medicineAcute pancreatitisPeroxiredoxinFree Radical Biology and Medicine
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Effects of Nrf2 deficiency on bone microarchitecture in an experimental model of osteoporosis

2014

Objective. Redox imbalance contributes to bone fragility. We have evaluated the in vivo role of nuclear factor erythroid derived 2-related factor-2 (Nrf2), an important regulator of cellular responses to oxidative stress, in bone metabolism using a model of postmenopausal osteoporosis. Methods. Ovariectomy was performed in both wild-type and mice deficient in Nrf2 (Nrf2-/-). Bone microarchitecture was analyzed by CT. Serum markers of bone metabolism were also measured. Reactive oxygen species production was determined using dihydrorhodamine 123. Results. Sham-operated or ovariectomized Nrf2 -/- mice exhibit a loss in trabecular bone mineral density in femur, accompanied by a reduction in co…

Agingmedicine.medical_specialtycytoarchitectureArticle SubjectNF-E2-Related Factor 2MedicinaOsteoporosisOsteoclastsBone Marrow Cellsprotein deficiencymedicine.disease_causeenvironment and public healthBiochemistryBone resorptionBone remodelingMiceIn vivoInternal medicinemedicineAnimalsFemurcontrolled studyFemurlcsh:QH573-671Cells CulturedMice Knockoutchemistry.chemical_classificationReactive oxygen specieslcsh:CytologyChemistrybone densityCell DifferentiationCell BiologyGeneral Medicinerespiratory systemmedicine.diseaseosteoporosisMice Inbred C57BLDisease Models AnimalOxidative StressEndocrinologyOvariectomized ratReactive Oxygen SpeciesTomography X-Ray ComputedBiomarkersOxidative stressResearch Article
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Heme oxygenase-1 induction modulates microsomal prostaglandin E synthase-1 expression and prostaglandin E2 production in osteoarthritic chondrocytes

2009

Pro-inflammatory cytokines such as interleukin-1beta (IL-1beta) may participate in the pathogenesis of cartilage damage in osteoarthritis (OA) through the production of catabolic enzymes and inflammatory mediators. Induction of heme oxygenase-1 (HO-1) has previously been shown to exert anti-inflammatory effects in different cell types. We have investigated whether HO-1 induction may modify chondrocyte viability and the production of relevant mediators such as oxidative stress and prostaglandin E(2) (PGE(2)) elicited by IL-1beta in OA chondrocytes. Chondrocytes were isolated from OA cartilage and used in primary culture. Cells were stimulated with IL-1beta in the absence or presence of the H…

Transcriptional Activationmedicine.medical_specialtyCell Survivalmedicine.medical_treatmentBiologymedicine.disease_causeProstaglandin E synthaseBiochemistryDinoprostoneChondrocyteChondrocytesMicrosomesInternal medicineOsteoarthritismedicineHumansProstaglandin E2Cells CulturedAggrecanProstaglandin-E SynthasesPharmacologyCOPPMolecular biologyIntramolecular OxidoreductasesHeme oxygenasemedicine.anatomical_structureEndocrinologybiology.proteinHeme Oxygenase-1Oxidative stressProstaglandin Emedicine.drugBiochemical Pharmacology
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

2021

Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to…

0301 basic medicineProgrammed cell deathSettore BIO/06AutophagosomeAutolysosome[SDV]Life Sciences [q-bio]lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Autophagy-Related ProteinsReviewComputational biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologySettore MED/0403 medical and health sciencesstressChaperone-mediated autophagyddc:570AutophagyLC3AnimalsHumanscancerSettore BIO/10Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSet (psychology)Molecular Biologyvacuole.phagophore030102 biochemistry & molecular biologyvacuolebusiness.industryInterpretation (philosophy)AutophagyAutophagosomesneurodegenerationCell BiologyfluxMulticellular organismmacroautophagy030104 developmental biologyKnowledge baselysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleBiological AssayLysosomesbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Autophagy

2021

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide…

macroautophagy;autophagyAutophagosome[SDV]Life Sciences [q-bio]canceLC3 macroautophagyautophagosomeneurodegeneration;[SDV.BC]Life Sciences [q-bio]/Cellular BiologyAutophagy AutophagosomeNOstress vacuolestressautophagic processesstrerfluxLC3cancerguidelinesAutophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/06 - Anatomia Comparata E Citologia[SDV.BC] Life Sciences [q-bio]/Cellular BiologyComputingMilieux_MISCELLANEOUSMedaka oryzias latipesphagophorevacuoleQHneurodegenerationAutophagosome cancer flux LC3 lysosome macroautophagy neurodegeneration phagophore stress vacuoleautophagy; autophagic processes; guidelines; autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuolefluxmacroautophagystress.lysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/17 - ISTOLOGIARC
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European contribution to the study of ROS : A summary of the findings and prospects for the future from the COST action BM1203 (EU-ROS)

2017

WOS: 000410470000009

0301 basic medicinereactive oxygen species ; reactive nitrogen species ; redox signaling ; oxidative stress ; antioxidants ; redox therapeuticsRedox signalingInternational CooperationSMOOTH-MUSCLE-CELLS[SDV]Life Sciences [q-bio]Clinical BiochemistryISCHEMIA-REPERFUSION INJURYReviewddc:616.07Bioinformaticsmedicine.disease_causeBiochemistryAntioxidants0302 clinical medicineENDOPLASMIC-RETICULUM STRESSCost actionlcsh:QH301-705.5ComputingMilieux_MISCELLANEOUSmedia_commonlcsh:R5-920Redox therapeuticsReactive nitrogen species3. Good healthVariety (cybernetics)MANGANESE SUPEROXIDE-DISMUTASECHRONIC GRANULOMATOUS-DISEASERisk analysis (engineering)ddc:540lcsh:Medicine (General)Oxidation-ReductionSignal TransductionSocieties ScientificPULMONARY ARTERIAL-HYPERTENSIONMedicinaEstrès oxidatiuBiology03 medical and health sciencesAntioxidants ; Oxidative Stress ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Redox Signaling ; Redox TherapeuticsJournal Articlemedicinemedia_common.cataloged_instanceAnimalsHumans[CHIM]Chemical SciencesEuropean UnionEuropean unionNITRIC-OXIDE SYNTHASETANDEM MASS-SPECTROMETRYMolecular BiologyMITOCHONDRIAL OXIDATIVE STRESSGROWTH-FACTOR-BETAOrganic ChemistryDisease progressionBiology and Life SciencesOxidation reductionManganese Superoxide Dismutase030104 developmental biologylcsh:Biology (General)Oxidative stressReactive oxygen species030217 neurology & neurosurgeryOxidative stressRedox biology
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