Search results for "ToP"

showing 10 items of 17685 documents

Mcl-1 targeting could be an intriguing perspective to cure cancer

2018

The Bcl-2 family, which plays important roles in controlling cancer development, is divided into antiapoptotic and proapoptotic members. The change in the balance between these members governs the life and death of the cells. Mcl-1 is an antiapoptotic member of this family and its distribution in normal and cancerous tissues strongly differs from that of Bcl-2. In human cancers, where upregulation of antiapoptotic proteins is common, Mcl-1 expression is regulated independent of Bcl-2 and its inhibition promotes senescence, a major barrier to tumorigenesis. Cancer chemotherapy determines various kinds of responses, such as senescence and autophagy; however, the ideal response to chemotherapy…

0301 basic medicineCarcinogenesisPhysiologyClinical BiochemistryApoptosisBiologymedicine.disease_causecancer care03 medical and health sciencesMcl-1 in cancer0302 clinical medicineBcl-2 familyimmune system diseasesCancer stem cellhemic and lymphatic diseasesNeoplasmsmedicinecancer-stem-cellHumansPost-translational regulationMolecular Targeted TherapyneoplasmsCellular SenescenceOncogeneBcl-2 familyAutophagyCancerCell Biologymedicine.diseaseMcl-1 isoformGene Expression Regulation Neoplastic030104 developmental biologyUSP9XProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisCancer researchtargeting Mcl-1Myeloid Cell Leukemia Sequence 1 ProteinCarcinogenesisProtein Processing Post-Translational
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Cardioprotection and natural polyphenols: An update of clinical and experimental studies

2018

Myocardial ischemia is the leading cause of death worldwide. Despite better outcomes with early coronary artery reperfusion strategies, morbidity and mortality remain significant. The principal myocardial hallmark of myocardial ischemia is cell death and the associated impairment of cardiac contractility. In this way, the use of extracts from medicinal plants versus synthetic drugs to mitigate post-ischemic damage constitutes an alternative. Despite their proven beneficial effects in cardiovascular disorders, the use of many plants is questioned. Our aim is to update the clinical and experimental studies about the actions of medicinal plants and polyphenol-enriched extracts against ischemia…

0301 basic medicineCardiotonic AgentsMyocardial ischemiaCIENCIAS MÉDICAS Y DE LA SALUDMyocardial IschemiaMEDLINE030204 cardiovascular system & hematologyFisiologíaNATURAL PRODUCTS03 medical and health sciencesISCHEMIA-REPERFUSIONCARDIOPROTECTION0302 clinical medicineWeb of knowledgeMITOCHONDRIAAnimalsHumansMedicineCardioprotective AgentMedicinal plantsBeneficial effectsCause of deathCardioprotectionClinical Trials as TopicTraditional medicinePlant Extractsbusiness.industryPolyphenolsfood and beveragesGeneral MedicineMedicina Básica030104 developmental biologybusinessFood Science
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CD40/CD40L and Related Signaling Pathways in Cardiovascular Health and Disease—The Pros and Cons for Cardioprotection

2020

The CD40–CD40 ligand (CD40L) dyad represents a scientific and clinical field that has raised many controversies in the past and cannot be clearly defined as being an either beneficial or harmful pathway. Being crucially involved in physiological immunological processes as well as pathological inflammatory reactions, the signaling pathway has been recognized as a key player in the development of both autoimmune and cardiovascular disease. Even though the possibilities of a therapeutic approach to the dyad were recognized decades ago, due to unfortunate events, detailed in this review, pharmacological treatment targeting the dyad, especially in patients suffering from atherosclerosis, is not …

0301 basic medicineCardiovascular healthMice TransgenicInflammationReviewDisease030204 cardiovascular system & hematologyBioinformaticsCardiovascular SystemCatalysisAutoimmune DiseasesInorganic Chemistrylcsh:ChemistryMice03 medical and health sciencesTherapeutic approach0302 clinical medicineRisk Factorscardiovascular diseaseDiabetes mellitusCD40AnimalsHumansMedicineGene SilencingCD40 AntigensPhysical and Theoretical ChemistryMolecular Biologylcsh:QH301-705.5SpectroscopyCardioprotectionClinical Trials as Topicbusiness.industryOrganic ChemistryGeneral Medicinemedicine.diseaseComputer Science Applications030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Cardiovascular DiseasesinflammationCd40 cd40lSignal transductionmedicine.symptomCD40 ligandatherosclerosisbusinessSignal TransductionInternational Journal of Molecular Sciences
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Infrared microspectroscopic determination of collagen cross-links in articular cartilage

2017

Collagen forms an organized network in articular cartilage to give tensile stiffness to the tissue. Due to its long half-life, collagen is susceptible to cross-links caused by advanced glycation end-products. The current standard method for determination of cross-link concentrations in tissues is the destructive high-performance liquid chromatography (HPLC). The aim of this study was to analyze the cross-link concentrations nondestructively from standard unstained histological articular cartilage sections by using Fourier transform infrared (FTIR) microspectroscopy. Half of the bovine articular cartilage samples ( n = 27 ) were treated with threose to increase the collagen cross-linking whi…

0301 basic medicineCartilage ArticularGlycation End Products AdvancedcollagenSpectrophotometry InfraredPROTEOGLYCAN01 natural sciencesHigh-performance liquid chromatographychemistry.chemical_compoundBiomedicinsk laboratorievetenskap/teknologiPartial least squares regressionBiomedical Laboratory Science/Technologyinfrared spectroscopyPyridinolineThreoseChemistryMedicinsk bildbehandlingSTIFFNESSinfrapunaspektroskopiata3141AnatomyAtomic and Molecular Physics and OpticsDIFFUSIONElectronic Optical and Magnetic Materialsmedicine.anatomical_structuremultivariate analysisGLYCATION END-PRODUCTSNONENZYMATIC GLYCATIONBiomedical EngineeringInfrared spectroscopyI COLLAGENFORMALIN FIXATIONcross-linksOrthopaedicsBiomaterials03 medical and health sciencesmedicineAnimalsarticular cartilageFourier transform infrared spectroscopyPentosidineLeast-Squares Analysista217ChromatographyCartilage010401 analytical chemistry3126 Surgery anesthesiology intensive care radiology0104 chemical sciencesMedical Image Processing030104 developmental biologyOrtopedi1182 Biochemistry cell and molecular biologyCattleJournal of Biomedical Optics
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Extracellular histones activate autophagy and apoptosis via mTOR signaling in human endothelial cells.

2018

Circulating histones have been proposed as targets for therapy in sepsis and hyperinflammatory symptoms. However, the proposed strategies have failed in clinical trials. Although different mechanisms for histone-related cytotoxicity are being explored, those mediated by circulating histones are not fully understood. Extracellular histones induce endothelial cell death, thereby contributing to the pathogenesis of complex diseases such as sepsis and septic shock. Therefore, the comprehension of cellular responses triggered by histones is capital to design effective therapeutic strategies. Here we report how extracellular histones induce autophagy and apoptosis in a dose-dependent manner in cu…

0301 basic medicineCell SurvivalEndothelial cellsFisiologiaApoptosisAMP-Activated Protein KinasesHistones03 medical and health sciencesExtracellularAutophagyHuman Umbilical Vein Endothelial CellsAutophagy-Related Protein-1 HomologHumansMolecular BiologyProtein kinase BPI3K/AKT/mTOR pathwaybiologyDose-Response Relationship DrugChemistryTOR Serine-Threonine KinasesAutophagyIntracellular Signaling Peptides and ProteinsAMPKNuclear ProteinsCirculating histonesCell biologyToll-like receptorsEndothelial stem cell030104 developmental biologyHistoneApoptosisbiology.proteinMolecular MedicineProto-Oncogene Proteins c-aktSignal TransductionBiochimica et biophysica acta. Molecular basis of disease
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Indomethacin Disrupts Autophagic Flux by Inducing Lysosomal Dysfunction in Gastric Cancer Cells and Increases Their Sensitivity to Cytotoxic Drugs

2018

AbstractNSAIDs inhibit tumorigenesis in gastrointestinal tissues and have been proposed as coadjuvant agents to chemotherapy. The ability of cancer epithelial cells to adapt to the tumour environment and to resist cytotoxic agents seems to depend on rescue mechanisms such as autophagy. In the present study we aimed to determine whether an NSAID with sensitizing properties such as indomethacin modulates autophagy in gastric cancer epithelial cells. We observed that indomethacin causes lysosomal dysfunction in AGS cells and promotes the accumulation of autophagy substrates without altering mTOR activity. Indomethacin enhanced the inhibitory effects of the lysosomotropic agent chloroquine on l…

0301 basic medicineCell SurvivalIndomethacinlcsh:MedicineAntineoplastic AgentsAdenocarcinomaArticle03 medical and health sciencesStomach NeoplasmsCell Line TumorLysosomeAutophagymedicineHumansCytotoxic T cellViability assayCytotoxicitylcsh:SciencePI3K/AKT/mTOR pathwayAnalysis of VarianceMultidisciplinaryCell DeathChemistryAnti-Inflammatory Agents Non-SteroidalAutophagylcsh:RChloroquineDrug SynergismOxaliplatin030104 developmental biologymedicine.anatomical_structureDrug Resistance NeoplasmApoptosisCancer cellCancer researchlcsh:QMacrolidesLysosomesScientific Reports
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New insights into the mechanism of action of pyrazolo[1,2-a]benzo[1,2,3,4]tetrazin-3-one derivatives endowed with anticancer potential

2018

Due to the scarce biological profile, the pyrazolo[1,2-a]benzo[1,2,3,4]tetrazine-3-one scaffold (PBT) has been recently explored as promising core for potential anticancer candidates. Several suitably decorated derivatives (PBTs) exhibited antiproliferative activity in the low-micromolar range associated with apoptosis induction and cell cycle arrest on S phase. Herein, we selected the most active derivatives and submitted them to further biological explorations to deepen the mechanism of action. At first, a DNA targeting is approached by means of flow Linear Dichroism experiments so as to evaluate how small planar molecules might interact with DNA, including the interference with the catal…

0301 basic medicineCell cycle checkpointPyrazolo[1TetrazolesBiochemistrychemistry.chemical_compound0302 clinical medicineSalmonAntiproliferative; DNA-interacting; Intercalation; Linear dichroism; Molecular docking; Pyrazolo[12-a]benzo[1234]tetrazin-3-one; Topoisomerase II; Biochemistry; Molecular MedicineDrug DiscoveryDNA-interactingBase PairingADMEbiologyIntercalating AgentsMolecular Docking Simulation030220 oncology & carcinogenesisMolecular Medicinemedicine.symptomtopoisomerase II3StereochemistryIn silico2Antineoplastic Agentslinear dichroism03 medical and health sciencesantiproliferativeintercalationmedicineAnimalsHumansDNA Cleavage2-a]benzo[1Pharmacology4]tetrazin-3-oneBinding SitesTopoisomeraseOrganic ChemistryDNAmolecular dockingSettore CHIM/08 - Chimica FarmaceuticaChemical spaceProtein Structure TertiaryDNA Topoisomerases Type II030104 developmental biologyMechanism of actionchemistryCatalytic cyclebiology.proteinpyrazolo[12-a]benzo[1234]tetrazin-3-oneDNAChemical Biology & Drug Design
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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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L-carnitine protects C2C12 cells against mitochondrial superoxide overproduction and cell death.

2017

International audience; AIMTo identify and characterize the protective effect that L-carnitine exerted against an oxidative stress in C2C12 cells.METHODSMyoblastic C2C12 cells were treated with menadione, a vitamin K analog that engenders oxidative stress, and the protective effect of L-carnitine (a nutrient involved in fatty acid metabolism and the control of the oxidative process), was assessed by monitoring various parameters related to the oxidative stress, autophagy and cell death.RESULTSAssociated with its physiological function, a muscle cell metabolism is highly dependent on oxygen and may produce reactive oxygen species (ROS), especially under pathological conditions. High levels o…

0301 basic medicineCell deathProgrammed cell deathMitochondrial superoxideMitochondrion03 medical and health sciences0302 clinical medicineSuperoxide anionsCarnitinemedicineCarnitineOverproductionOxygen specieschemistry.chemical_classificationReactive oxygen species[ SDV.IDA ] Life Sciences [q-bio]/Food engineeringBasic Studymusculoskeletal systemReactive AutophagyCell biologyMitochondria030104 developmental biologychemistryMuscletissuesC2C12030217 neurology & neurosurgerymedicine.drugWorld journal of biological chemistry
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Autophagy in the pathogenesis of ankylosing spondylitis

2016

The pathogenesis of ankylosing spondylitis (AS) is not well understood, and treatment options have met with limited success. Autophagy is a highly conserved mechanism of controlled digestion of damaged organelles within a cell. It helps in the maintenance of cellular homeostasis. The process of autophagy requires the formation of an isolation membrane. They form double-membraned vesicles called “autophagosomes” that engulf a portion of the cytoplasm. Beyond the role in maintenance of cellular homeostasis, autophagy has been demonstrated as one of the most remarkable tools employed by the host cellular defense against bacteria invasion. Autophagy also affects the immune system and thus is im…

0301 basic medicineCellAutophagy-Related ProteinsATG16L1Cellular homeostasisInflammationBiologyLeucine-Rich Repeat Serine-Threonine Protein Kinase-2Pathogenesis03 medical and health sciencesImmune systemRheumatologyATG16L1; Autophagy; Inflammation; LRRK2; Pathogenesis; Spondyloarthritis; RheumatologyPathogenesiAutophagymedicineHomeostasisHumansSpondylitis AnkylosingATG16L1InflammationAutophagyLRRK2General MedicineCell biology030104 developmental biologymedicine.anatomical_structureCytoplasmSpondyloarthritimedicine.symptomClinical Rheumatology
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