Search results for "Stress."

showing 10 items of 5934 documents

Magnesium and Other Biometals in Oxidative Medicine and Redox Biology

2017

No abstract available.

0301 basic medicineCell Biology magnesiumAgingSettore MED/09 - Medicina InternaArticle Subjectchemistry.chemical_elementOxidative phosphorylationBiologyBiochemistryRedox03 medical and health sciencesAnimalsHumansMagnesiumBiochemistry; Aging; Cell Biology magnesiumlcsh:QH573-671Magnesiumlcsh:CytologyCell BiologyGeneral MedicineTrace ElementsOxidative Stress030104 developmental biologyEditorialchemistryBiochemistryOxidation-ReductionOxidative Medicine and Cellular Longevity
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CHK1 inhibitor sensitizes resistant colorectal cancer stem cells to nortopsentin

2021

Summary Limited therapeutic options are available for advanced colorectal cancer (CRC). Herein, we report that exposure to a neo-synthetic bis(indolyl)thiazole alkaloid analog, nortopsentin 234 (NORA234), leads to an initial reduction of proliferative and clonogenic potential of CRC sphere cells (CR-CSphCs), followed by an adaptive response selecting the CR-CSphC-resistant compartment. Cells spared by the treatment with NORA234 express high levels of CD44v6, associated with a constitutive activation of Wnt pathway. In CR-CSphC-based organoids, NORA234 causes a genotoxic stress paralleled by G2-M cell cycle arrest and activation of CHK1, driving the DNA damage repair of CR-CSphCs, regardless…

0301 basic medicineCell cycle checkpointColorectal cancerScienceSettore MED/50 - Scienze Tecniche Mediche Applicate02 engineering and technologyGenotoxic StressArticleMolecular Physiology03 medical and health sciencesSettore MED/04 - PATOLOGIA GENERALERabusertibmedicineClonogenic assayCancerMultidisciplinarybusiness.industryQWnt signaling pathwayDrugsCancerCell Biology021001 nanoscience & nanotechnologymedicine.disease030104 developmental biologyCancer researchSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratorioStem cell0210 nano-technologybusinesscolorectal cancer cancer stem cells alkaloids DNA damage repair CHK1.iScience
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Integrated molecular signaling involving mitochondrial dysfunction and alteration of cell metabolism induced by tyrosine kinase inhibitors in cancer.

2020

Cancer cells have unlimited replicative potential, insensitivity to growth-inhibitory signals, evasion of apoptosis, cellular stress, and sustained angiogenesis, invasiveness and metastatic potential. Cancer cells adequately adapt cell metabolism and integrate several intracellular and redox signaling to promote cell survival in an inflammatory and hypoxic microenvironment in order to maintain/expand tumor phenotype. The administration of tyrosine kinase inhibitor (TKI) constitutes the recommended therapeutic strategy in different malignancies at advanced stages. There are important interrelationships between cell stress, redox status, mitochondrial function, metabolism and cellular signali…

0301 basic medicineCell deathCell signalingClinical BiochemistryPGC-1αApoptosisReview ArticleBiochemistryReceptor tyrosine kinase03 medical and health sciencesPhosphatidylinositol 3-Kinases0302 clinical medicineNeoplasmsAutophagyTumor MicroenvironmentHumansProtein kinase AProtein kinase Blcsh:QH301-705.5Protein Kinase InhibitorsPI3K/AKT/mTOR pathwaylcsh:R5-920biologyOrganic ChemistryMitochondria030104 developmental biologylcsh:Biology (General)Redox statusCancer cellbiology.proteinCancer researchEndoplasmic reticulum stressmTORSignal transductionlcsh:Medicine (General)Tyrosine kinaseProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryRedox biology
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The Double-Edged Sword Profile of Redox Signaling: Oxidative Events As Molecular Switches in the Balance between Cell Physiology and Cancer.

2018

The intracellular redox state in the cell depends on the balance between the level of reactive oxygen species (ROS) and the activity of defensive systems including antioxidant enzymes. This balance is a dynamic process that can change in relation to many factors and/or stimuli induced within the cell. ROS production is derived from physiological metabolic events. For instance, mitochondria represent the major ROS sources during oxidative phosphorylation, but other systems, such as NADPH oxidase or specific enzymes in certain metabolisms, may account for ROS production as well. Whereas high levels of ROS perturb the cell environment, causing oxidative damage to biological macromolecules, low…

0301 basic medicineCell physiologyOxidative phosphorylationMitochondrionToxicologymedicine.disease_cause03 medical and health sciencesOxidative Stress ROS antioxidant systems0302 clinical medicineNeoplasmsmedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistryNADPH OxidasesGeneral MedicineCell biology030104 developmental biology030220 oncology & carcinogenesisbiology.proteinSignal transductionReactive Oxygen SpeciesOxidation-ReductionIntracellularOxidative stressSignal TransductionChemical research in toxicology
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The Role of Nrf2 and PPARγ in the Improvement of Oxidative Stress in Hypertension and Cardiovascular Diseases

2020

Reactive oxygen species are an important element of redox regulation in cells and tissues. During physiological processes, molecules undergo chemical changes caused by reduction and oxidation reactions. Free radicals are involved in interactions with other molecules, leading to oxidative stress. Oxidative stress works two ways depending on the levels of oxidizing agents and products. Excessive action of oxidizing agents damages biomolecules, while a moderate physiological level of oxidative stress (oxidative eustress) is necessary to control life processes through redox signaling required for normal cellular operation. High levels of reactive oxygen species (ROS) mediate pathological change…

0301 basic medicineCell signalingNF-E2-Related Factor 2PhysiologyBlood PressureReviewOxidative phosphorylationmedicine.disease_cause03 medical and health sciences0302 clinical medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwaychemistry.chemical_classificationReactive oxygen speciesKelch-Like ECH-Associated Protein 1ChemistryGeneral MedicineKEAP1Antioxidant Response ElementsNFE2L2Cell biologyPPAR gammaOxidative Stress030104 developmental biologyCardiovascular DiseasesHypertensionReactive Oxygen Species030217 neurology & neurosurgeryOxidative stressSignal TransductionPhysiological Research
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Circadian Rhythm in Adipose Tissue: Novel Antioxidant Target for Metabolic and Cardiovascular Diseases

2020

Obesity is a major risk factor for most metabolic and cardiovascular disorders. Adipose tissue is an important endocrine organ that modulates metabolic and cardiovascular health by secreting signaling molecules. Oxidative stress is a common mechanism associated with metabolic and cardiovascular complications including obesity, type 2 diabetes, and hypertension. Oxidative stress can cause adipose tissue dysfunction. Accumulating data from both humans and experimental animal models suggest that adipose tissue function and oxidative stress have an innate connection with the intrinsic biological clock. Circadian clock orchestrates biological processes in adjusting to daily environmental changes…

0301 basic medicineCell signalingPhysiologyClinical BiochemistryCircadian clockAdipose tissueAdipokineReviewBioinformaticsmedicine.disease_causeBiochemistrysirtuin 103 medical and health sciences0302 clinical medicineAdipokinesclock genesMedicineoxidative stressCircadian rhythmbranched-chain amino acidsMolecular Biologyendothelial nitric oxide synthasebiologySirtuin 1business.industrylcsh:RM1-950Cell BiologyCLOCK030104 developmental biologylcsh:Therapeutics. Pharmacologybiology.proteinbusiness030217 neurology & neurosurgeryOxidative stressAntioxidants
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Oxidative Stress and Vascular Dysfunction in the Retina: Therapeutic Strategies

2020

Many retinal diseases, such as diabetic retinopathy, glaucoma, and age-related macular (AMD) degeneration, are associated with elevated reactive oxygen species (ROS) levels. ROS are important intracellular signaling molecules that regulate numerous physiological actions, including vascular reactivity and neuron function. However, excessive ROS formation has been linked to vascular endothelial dysfunction, neuron degeneration, and inflammation in the retina. ROS can directly modify cellular molecules and impair their function. Moreover, ROS can stimulate the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) causing inflammation and cel…

0301 basic medicineCell signalingProgrammed cell deathPhysiologyClinical BiochemistryInflammationReviewmedicine.disease_causeBiochemistryProinflammatory cytokine03 medical and health sciences0302 clinical medicinemedicineoxidative stressEndothelial dysfunctionMolecular Biologyreactive oxygen speciesRetinabusiness.industrylcsh:RM1-950Cell Biologymedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacology030221 ophthalmology & optometryTumor necrosis factor alpharetinal diseasemedicine.symptombusinessvascular endotheliumOxidative stressAntioxidants
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Bifidobacterium CECT 7765 modulates early stress-induced immune, neuroendocrine and behavioral alterations in mice.

2016

Emerging evidence suggests that there is a window of opportunity within the early developmental period, when microbiota-based interventions could play a major role in modulating the gut-brain axis and, thereby, in preventing mood disorders. This study aims at evaluating the effects and mode of action of Bifidobacterium pseudocatenulatum CECT 7765 in a murine model of chronic stress induced by maternal separation (MS). C57Bl/6J male breast-fed pups were divided into four groups, which were subjected or not to MS and supplemented with placebo or B. pseudocatenulatum CECT7765 until postnatal period (P) 21 and followed-up until P41. Behavioral tests were performed and neuroendocrine parameters …

0301 basic medicineCentral Nervous SystemMalemedicine.medical_specialtyHypothalamo-Hypophyseal Systemmedicine.medical_treatmentImmunologyBifidobacterium pseudocatenulatumPituitary-Adrenal SystemInflammationBiologyDiet High-Fat03 medical and health sciencesBehavioral Neurosciencechemistry.chemical_compoundMice0302 clinical medicineImmune systemCorticosteroneStress PhysiologicalInternal medicineRNA Ribosomal 16SmedicineAnimalsChronic stressObesityNeurotransmitterInflammationNeurotransmitter AgentsEndocrine and Autonomic SystemsMaternal DeprivationMicrobiotaProbioticsNeurosecretory SystemsIntestinesMice Inbred C57BL030104 developmental biologyCytokineEndocrinologychemistryHypothalamusImmunologyDietary SupplementsCytokinesBifidobacteriummedicine.symptom030217 neurology & neurosurgeryBrain, behavior, and immunity
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The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.

2019

Friedreich’s ataxia (FRDA) is a rare early-onset degenerative disease that affects both the central and peripheral nervous systems, and other extraneural tissues, mainly the heart and endocrine pancreas. This disorder progresses as a mixed sensory and cerebellar ataxia, primarily disturbing the proprioceptive pathways in the spinal cord, peripheral nerves and nuclei of the cerebellum. FRDA is an inherited disease with an autosomal recessive pattern caused by an insufficient amount of the nuclear-encoded mitochondrial protein frataxin, which is an essential and highly evolutionary conserved protein whose deficit results in iron metabolism dysregulation and mitochondrial dysfunction. The firs…

0301 basic medicineCerebellumAtaxiaFriedreich’s ataxiaReviewMitochondrionmedicine.disease_causelcsh:RC321-57103 medical and health sciencesiron0302 clinical medicineDegenerative diseasemedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationReactive oxygen speciesfrataxinbiologyCerebellar ataxialipid deregulationGeneral Neurosciencemedicine.diseaseanimal modelsCell biology030104 developmental biologymedicine.anatomical_structurechemistryFrataxinbiology.proteiniron chelatorsmedicine.symptom030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in neuroscience
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A Drosophila model of GDAP1 function reveals the involvement of insulin signalling in the mitochondria-dependent neuromuscular degeneration

2017

[EN] Charcot-Marie-Tooth disease is a rare peripheral neuropathy for which there is no specific treatment. Some forms of Charcot-Marie-Tooth are due to mutations in the GDAP1 gene. A striking feature of mutations in GDAP1 is that they have a variable clinical manifestation, according to disease onset and progression, histology and mode of inheritance. Studies in cellular and animal models have revealed a role of GDAP1 in mitochondrial morphology and distribution, calcium homeostasis and oxidative stress. To get a better understanding of the disease mechanism we have generated models of over-expression and RNA interference of the Drosophila Gdapl gene. In order to get an overview about the c…

0301 basic medicineCharcot-Marie-Toothmedicine.medical_treatmentNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_cause03 medical and health sciencesCharcot-Marie-Tooth DiseaseRNA interferenceGene expressionBIOQUIMICA Y BIOLOGIA MOLECULARmedicineAnimalsDrosophila ProteinsHumansInsulinMolecular BiologyGeneticsMechanism (biology)InsulinNeurodegenerationLipid Metabolismmedicine.diseaseUp-RegulationMitochondriaCell biology030104 developmental biologyMetabolomeCarbohydrate MetabolismMolecular MedicineDrosophilaRNA InterferenceOxidative stressFunction (biology)Signal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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