Search results for "CHON"

showing 10 items of 1866 documents

Aging-Related Disorders and Mitochondrial Dysfunction: A Critical Review for Prospect Mitoprotective Strategies Based on Mitochondrial Nutrient Mixtu…

2020

A number of aging-related disorders (ARD) have been related to oxidative stress (OS) and mitochondrial dysfunction (MDF) in a well-established body of literature. Most studies focused on cardiovascular disorders (CVD), type 2 diabetes (T2D), and neurodegenerative disorders. Counteracting OS and MDF has been envisaged to improve the clinical management of ARD, and major roles have been assigned to three mitochondrial cofactors, also termed mitochondrial nutrients (MNs), i.e., alpha-lipoic acid (ALA), Coenzyme Q10 (CoQ10), and carnitine (CARN). These cofactors exert essential-and distinct-roles in mitochondrial machineries, along with strong antioxidant properties. Clinical trials have mostly…

0301 basic medicineAgingAntioxidantUbiquinonemedicine.medical_treatmentmitochondrial nutrientsReviewoptic neuropathiesType 2 diabetesPharmacologyMitochondrionmedicine.disease_causeAntioxidantslcsh:Chemistrychemistry.chemical_compound0302 clinical medicineCardiovascular Diseaseoxidative stressaging-related disorderslcsh:QH301-705.5SpectroscopyThioctic AcidMitochondrial nutrientNeurodegenerative DiseasesGeneral MedicineComputer Science ApplicationsMitochondriaCardiovascular DiseasesAntioxidantmedicine.drugHumanCatalysisAging-related disorderCell LineInorganic Chemistry03 medical and health sciencesCarnitinemedicineAnimalsHumansMicrobiomeCarnitinePhysical and Theoretical ChemistryMolecular BiologyCoenzyme Q10business.industryAnimalOrganic ChemistryOxidative Stremedicine.diseaseClinical trial030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryDiabetes Mellitus Type 2MicrobiomeOptic neuropathiebusinessMitochondrial dysfunction030217 neurology & neurosurgeryOxidative stress
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Homocysteine Induces Apoptosis of Human Umbilical Vein Endothelial Cells via Mitochondrial Dysfunction and Endoplasmic Reticulum Stress

2017

Homocysteine- (Hcy-) induced endothelial cell apoptosis has been suggested as a cause of Hcy-dependent vascular injury, while the proposed molecular pathways underlying this process are unclear. In this study, we investigated the adverse effects of Hcy on human umbilical vein endothelial cells (HUVEC) and the underlying mechanisms. Our results demonstrated that moderate-dose Hcy treatment induced HUVEC apoptosis in a time-dependent manner. Furthermore, prolonged Hcy treatment increased the expression of NOX4 and the production of intracellular ROS but decreased the ratio of Bcl-2/Bax and mitochondrial membrane potential (MMP), resulting in the leakage of cytochrome c and activation of caspa…

0301 basic medicineAgingArticle SubjectApoptosis030204 cardiovascular system & hematologyTransfectionBiochemistryUmbilical vein03 medical and health sciences0302 clinical medicineRisk FactorsHuman Umbilical Vein Endothelial CellsHumanslcsh:QH573-671Protein kinase AEndoplasmic Reticulum Chaperone BiPHomocysteinebiologylcsh:CytologyKinaseEndoplasmic reticulumCytochrome cCell BiologyGeneral MedicineEndoplasmic Reticulum StressMitochondriaCell biology030104 developmental biologyApoptosiscardiovascular systemUnfolded protein responsebiology.proteinPhosphorylationResearch ArticleOxidative Medicine and Cellular Longevity
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Adult rat myelin enhances axonal outgrowth from neural stem cells.

2018

Axon regeneration after spinal cord injury (SCI) is attenuated by growth inhibitory molecules associated with myelin. We report that rat myelin stimulated the growth of axons emerging from rat neural progenitor cells (NPCs) transplanted into sites of SCI in adult rat recipients. When plated on a myelin substrate, neurite outgrowth from rat NPCs and from human induced pluripotent stem cell (iPSC)-derived neural stem cells (NSCs) was enhanced threefold. In vivo, rat NPCs and human iPSC-derived NSCs extended greater numbers of axons through adult central nervous system white matter than through gray matter and preferentially associated with rat host myelin. Mechanistic investigations excluded …

0301 basic medicineAgingNeuronalNudeMessengerNeurodegenerativeInbred C57BLRegenerative MedicineMedical and Health SciencesMyelinMiceNeural Stem CellsStem Cell Research - Nonembryonic - HumanCyclic AMPAxonPhosphorylationGray MatterInduced pluripotent stem cellExtracellular Signal-Regulated MAP KinasesSpinal Cord InjuryMyelin SheathInbred F344Neuronal growth regulator 1Stem Cell Research - Induced Pluripotent Stem Cell - HumanChemistryGeneral MedicineBiological SciencesWhite MatterNeural stem cellCell biologymedicine.anatomical_structureSpinal Cord5.1 PharmaceuticalsNeurologicalFemaleStem Cell Research - Nonembryonic - Non-HumanDevelopment of treatments and therapeutic interventionsPhysical Injury - Accidents and Adverse EffectsNeuriteCell Adhesion Molecules NeuronalCentral nervous systemNeuronal OutgrowthArticleWhite matter03 medical and health sciencesRats NudemedicineAnimalsHumansRNA MessengerStem Cell Research - Embryonic - HumanTraumatic Head and Spine InjuryTransplantationStem Cell Research - Induced Pluripotent Stem CellNeurosciencesStem Cell ResearchRats Inbred F344AxonsRatsMice Inbred C57BL030104 developmental biologynervous systemChondroitin Sulfate ProteoglycansRNACell Adhesion Molecules
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Targeting the Endoplasmic Reticulum Unfolded Protein Response to Counteract the Oxidative Stress-Induced Endothelial Dysfunction

2017

In endothelial cells, the tight control of the redox environment is essential for the maintenance of vascular homeostasis. The imbalance between ROS production and antioxidant response can induce endothelial dysfunction, the initial event of many cardiovascular diseases. Recent studies have revealed that the endoplasmic reticulum could be a new player in the promotion of the pro- or antioxidative pathways and that in such a modulation, the unfolded protein response (UPR) pathways play an essential role. The UPR consists of a set of conserved signalling pathways evolved to restore the proteostasis during protein misfolding within the endoplasmic reticulum. Although the first outcome of the U…

0301 basic medicineAgingProgrammed cell deathendocrine systemOxidative phosphorylationReview Articlemedicine.disease_causeEndoplasmic ReticulumBiochemistryINITIATION-FACTOR 2-ALPHA03 medical and health sciencesProgrammed cell-deathSELECTIVE-INHIBITIONProgrammed cell-death;TXNIP/NLRP3 INFLAMMASOME ACTIVATION; MITOCHONDRIAL ELECTRON-TRANSPORT; SPONTANEOUSLY HYPERTENSIVE-RATS; INITIATION-FACTOR 2-ALPHA; CORONARY-ARTERY FUNCTION; ER STRESS; SELECTIVE-INHIBITION; MESSENGER-RNA; TRANSMEMBRANE PROTEINmedicineHumansEndothelial dysfunctionlcsh:QH573-671TXNIP/NLRP3 INFLAMMASOME ACTIVATIONSPONTANEOUSLY HYPERTENSIVE-RATSEndothelial Cellbusiness.industrylcsh:CytologyEndoplasmic reticulumfungiEndothelial CellsOxidative StreCell BiologyGeneral MedicineAdaptive responseMITOCHONDRIAL ELECTRON-TRANSPORTER STRESSmedicine.diseaseCell biologyOxidative Stress030104 developmental biologyProteostasisTRANSMEMBRANE PROTEINUnfolded protein responseUnfolded Protein ResponsebusinessMESSENGER-RNAOxidative stressCORONARY-ARTERY FUNCTIONHumanOxidative Medicine and Cellular Longevity
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Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Estrogenic regulation of skeletal muscle proteome : a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy

2017

Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17b-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. We utilized muscle samples from 24 pre- and postmenopausal women to establish proteome-wide profiles, associated with the difference in age (30–34 years old vs. 54– 62 years old), men…

0301 basic medicineAgingnaisetlabel‐free protein quantitationProteomeAnabolismvaihdevuodetmedicine.medical_treatmentTwinsmenopausenano‐LC‐HD‐MSElihakset0302 clinical medicineSTRENGTHBRAIN315 Sport and fitness sciencesta315luustoINHIBITORHormone replacement therapy (menopause)ta3142MITOCHONDRIAL BIOGENESISMiddle AgedPostmenopauseMenopauseREPLACEMENThormone replacement therapyEditorialmedicine.anatomical_structurehormonihoitoHormonal therapyOriginal ArticleFemalemuscleswomenAdultestrogeenitnano-LC-HD-MSEEXPRESSIONmedicine.medical_specialtyBiologyestrogenic regulation03 medical and health sciencesmitochondrial functionInternal medicinemedicineHumansMuscle Skeletallabel-free protein quantitationmuscle proteomeAgedSkeletal muscleEstrogenslabel-free proteinquantitationOriginal ArticlesCell Biologyfunctional annotationmedicine.diseaseMiddle ageMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauselihasmassaSarcopeniaCELLS3111 BiomedicineEnergy Metabolismfemale muscle030217 neurology & neurosurgeryskeletal musclesHormone
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Longevity-related molecular pathways are subject to midlife “switch” in humans

2019

Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that oppos…

0301 basic medicineAgingved/biology.organism_classification_rank.speciesMuscle Fibers SkeletallihaksetTranscriptome0302 clinical medicineGene expressionGene Regulatory NetworksRNA-Seqmedia_commonCerebral CortexNeuronsreactive oxygen speciesihoTOR Serine-Threonine Kinasesmitochondrial complex 1LongevityBrainNon-coding RNAAlzheimer'sECSITCell biologytranskriptio (biologia)mTORRNA Long NoncodingOriginal ArticleaivotSignal TransductionAdultTranscriptional ActivationskinIn silicomedia_common.quotation_subjectLongevityBiology03 medical and health sciencesHumanslong noncoding RNAskeletal muscleModel organismGeneSirolimusved/biologyagingRNACell BiologyTwins MonozygoticOriginal Articles030104 developmental biologyikääntyminenRNATranscriptome030217 neurology & neurosurgery
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Tenofovir-induced toxicity in renal proximal tubular epithelial cells

2017

OBJECTIVE In-vivo studies suggest that mitochondria is involved in tenofovir (TFV)-induced renal toxicity, but the underlying mechanisms are still unclear. The aim of the present study was to assess the effects of TFV and its prodrug, TFV disoproxil fumarate, on mitochondrial function and cell survival/viability in a renal proximal tubular cell line. DESIGN AND METHODS We evaluated parameters of cellular proliferation/survival (cell count, cell cycle, viability) and mitochondrial function (oxygen consumption, mitochondrial membrane potential, reactive oxygen species production) in NRK-52E cells. Intracellular TFV was measured by HPLC and expression of antioxidant genes was analysed by real-…

0301 basic medicineAnti-HIV AgentsCell Survival030106 microbiologyImmunologyCellOxidative phosphorylationMitochondrionPharmacologyCell Line03 medical and health sciencesmedicineHumansImmunology and AllergyTenofovirCell Proliferationchemistry.chemical_classificationKidneyReactive oxygen speciesCell growthEpithelial Cellsmedicine.diseaseMitochondriaMitochondrial toxicity030104 developmental biologyInfectious Diseasesmedicine.anatomical_structurechemistryIntracellularAIDS
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Zinc oxide nanoparticles mediated cytotoxicity, mitochondrial membrane potential and level of antioxidants in presence of melatonin.

2017

Zinc oxide nanoparticles (ZnO NPs) are widely used in a variety of products and are currently being investigated for biomedical applications. However, they have the potential to interact with macromolecules like proteins, lipids and DNA within the cells which makes the safe biomedical application difficult. The toxicity of the ZnO NP is mainly attributed reactive oxygen species (ROS) generation. Different strategies like iron doping, polymer coating and external supply of antioxidants have been evaluated to minimize the toxic potential of ZnO NPs. Melatonin is a hormone secreted by the pineal gland with great antioxidant properties. The melatonin is known to protect cells from ROS inducing …

0301 basic medicineAntioxidantFree RadicalsCell Survivalmedicine.medical_treatment02 engineering and technologyNitric OxideBiochemistryAntioxidantsNitric oxideCell LineMelatonin03 medical and health sciencesPineal glandchemistry.chemical_compoundMiceStructural BiologymedicineAnimalsDrug InteractionsCytotoxicityMolecular BiologyMelatoninchemistry.chemical_classificationMembrane potentialMembrane Potential MitochondrialReactive oxygen speciesBrainGeneral Medicine021001 nanoscience & nanotechnology030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryToxicityNanoparticlesZinc Oxide0210 nano-technologyReactive Oxygen Specieshormones hormone substitutes and hormone antagonistsmedicine.drugInternational journal of biological macromolecules
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