Search results for " Mito"

showing 10 items of 895 documents

Selective p38α MAP kinase/MAPK14 inhibition in enzymatically modified LDL-stimulated human monocytes: implications for atherosclerosis.

2016

The first ATP-competitive p38α MAPK/MAPK14 inhibitor with excellent in vivo efficacy and selectivity, skepinone-L, is now available. We investigated the impact of selective p38α MAPK/MAPK14 inhibition on enzymatically modified LDL (eLDL) stimulated human monocytes with its implications for atherosclerosis. Among the different p38 MAPK isoforms, p38α/MAPK14 was the predominantly expressed and activated isoform in isolated human peripheral blood monocytes. Moreover, eLDL colocalized with macrophages positive for p38α MAPK/MAPK14 in human carotid endarterectomy specimens. Using the human leukemia cell line THP-1 and/or primary monocyte-derived macrophages, skepinone-L inhibited eLDL-induced ac…

0301 basic medicineAdultMaleChemokineMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesCD36CCL4Dibenzocycloheptenes030204 cardiovascular system & hematologyBiochemistryGene Expression Regulation EnzymologicMonocytesMitogen-Activated Protein Kinase 1403 medical and health sciences0302 clinical medicineCell Line TumorGeneticsHumansInterleukin 8Molecular BiologyFoam cellMAPK14AgedAged 80 and overCaspase 7biologyChemistryCaspase 3Cholesterol LDLAtherosclerosisMolecular biology030104 developmental biologyBiochemistryMitogen-activated protein kinasebiology.proteinFemaleBiotechnologyFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Mitochondrial DNA haplogroups J and T increase the risk of glioma.

2021

The presence of different sets of mitochondrial polymorphisms generated by the accumulation of mutations in different maternal lineages has allowed differentiating mitochondrial haplogroups in human populations. These polymorphisms, in turn, may have effects at the phenotypic level, considering a possible contribution of these germinal mutations to the development of certain diseases such as cancer. The main goal of the present study is to establish a possible association between mitochondrial haplogroups and the risk of suffering glioma. Blood samples were obtained from 32 patients from Catalonia (Spain) diagnosed with different grades of glioma (II, III and IV), according to the World Hea…

0301 basic medicineAdultMaleMitochondrial DNAPopulationBiologyDNA MitochondrialHaplogroup03 medical and health sciences0302 clinical medicineGliomamedicineHumansGenetic Predisposition to DiseaseeducationMolecular BiologyGeneticseducation.field_of_studyBrain NeoplasmsCancerCell BiologyGliomamedicine.diseasePhenotype030104 developmental biologyIncreased riskHaplotypesMolecular MedicineFemale030217 neurology & neurosurgeryHuman mitochondrial DNA haplogroupMitochondrion
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Obesity impairs leukocyte‐endothelium cell interactions and oxidative stress in humans

2018

Background:To evaluate the relationship between leukocyte‐endothelial cellinteractions and oxidative stress parameters in non‐diabetic patients with differentgrades of obesity.Material and methods:For this cross‐sectional study, 225 subjects wererecruited from January 1, 2014 to December 31, 2016 and divided into groupsaccording to BMI (40 kg/m²). We determined clin-ical parameters, systemic inflammatory markers, soluble cellular adhesion mole-cules, leukocyte‐endothelium cell interactions—rolling flux, velocity and adhesion—, oxidative stress parameters—total ROS, total superoxide, glutathione—andmitochondrial membrane potential in leukocytes.Results:We verified that HOMA‐IR and hsCRP incr…

0301 basic medicineAdultMalemedicine.medical_specialtyEndotheliumAdolescentClinical BiochemistryCell Communication030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causeBiochemistryProinflammatory cytokineBody Mass Index03 medical and health sciencesYoung Adult0302 clinical medicineInternal medicinemedicineCell AdhesionLeukocytesHumansObesityEndothelial dysfunctionCell adhesionAgedchemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesChemistryCell adhesion moleculeEndothelial CellsGeneral MedicineMiddle AgedAtherogenesismedicine.diseaseIntercellular Adhesion Molecule-1Oxidative Stress030104 developmental biologyEndocrinologymedicine.anatomical_structureCross-Sectional StudiesCytokinesReactive oxygen specieFemaleMitochondrial membrane potentialReactive Oxygen SpeciesOxidative stress
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Mechanisms of action of metformin in type 2 diabetes: Effects on mitochondria and leukocyte-endothelium interactions.

2020

Type 2 diabetes (T2D) is a very prevalent, multisystemic, chronic metabolic disorder closely related to atherosclerosis and cardiovascular diseases. It is characterised by mitochondrial dysfunction and the presence of oxidative stress. Metformin is one of the safest and most effective anti-hyperglycaemic agents currently employed as first-line oral therapy for T2D. It has demonstrated additional beneficial effects, unrelated to its hypoglycaemic action, on weight loss and several diseases, such as cancer, cardiovascular disorders and metabolic diseases, including thyroid diseases. Despite the vast clinical experience gained over several decades of use, the mechanism of action of metformin i…

0301 basic medicineAdvanced glycation end product (AGE)AMP-activated protein kinase (AMPK)endocrine system diseasesglycerol 3-phosphate dehydrogenase (GPD)Clinical Biochemistrytype 1 diabetes (T1D)Type 2 diabetesmTORC1Review Articleelectron transport chain (ETC)PharmacologyMitochondrionmedicine.disease_causeBiochemistry0302 clinical medicineLeukocytesCREB-binding protein (CBP)inner mitochondrial membrane (IMM)lcsh:QH301-705.5lcsh:R5-920cAMP response element-binding (CREB)glucagon-like peptide 1 (GLP-1)type 2 diabetes (T2D)Type 2 diabetesMetforminMetforminMitochondriamedicine.anatomical_structurereactive nitrogen species (RNS)reactive oxygen species (ROS)sirtuin (SIRT)medicine.symptomlcsh:Medicine (General)cardiovascular diseases (CVD)medicine.drugEndotheliumnitric oxide synthase (NOS)polycystic ovary syndrome (PCOS)Pathophysiologyinsulin resistance (IR)superoxide dismutase (SOD)03 medical and health sciencesglycated haemoglobin (HbA1c)medicineorganic cation transporter (OCT)HumansEndotheliumintercellular adhesion molecule-1 (ICAM-1)business.industryoxidative phosphorylation (OXPHOS)Organic Chemistryperoxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)AMPKmedicine.diseaseAtherosclerosisvascular cell adhesion molecule-1 (VCAM-1)Treatment030104 developmental biologylcsh:Biology (General)Mechanism of actionDiabetes Mellitus Type 2Oxidative stressbusinessinsulin receptor substrate (IRS)030217 neurology & neurosurgeryOxidative stress
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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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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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Redox Imbalance and Mitochondrial Release of Apoptogenic Factors at the Forefront of the Antitumor Action of Mango Peel Extract

2021

Today, an improved understanding of cancer cell response to cellular stress has become more necessary. Indeed, targeting the intracellular pro-oxidant/antioxidant balance triggering the tumor commitment to cell demise could represent an advantageous strategy to develop cancer-tailored therapies. In this scenario, the present study shows how the peel extract of mango—a tropical fruit rich in phytochemicals with nutraceutical properties—can affect the cell viability of three colon cancer cell lines (HT29, Caco-2 and HCT116), inducing an imbalance of cellular redox responses. By using hydro-alcoholic mango peel extract (MPE), we observed a consistent decline in thiol group content, which was a…

0301 basic medicineAntioxidantmedicine.medical_treatmentCellPharmaceutical ScienceOrganic chemistryApoptosisphytochemicalArticleAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineQD241-441Downregulation and upregulationCell Line TumorNeoplasmsDrug DiscoverymedicineHumansViability assayPhysical and Theoretical ChemistryMethyl gallateMembrane Potential MitochondrialMangiferaPlant Extractsmitochondrial apoptogenic proteinsphytochemicalsAntineoplastic Agents PhytogenicBcl-2 family proteinCell biologyMitochondriaBcl-2 family proteins030104 developmental biologymedicine.anatomical_structurechemistryChemistry (miscellaneous)030220 oncology & carcinogenesisCancer cellMolecular MedicineVDAC1Oxidation-ReductionIntracellularmitochondria injuryMolecules
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Regulation of vascular function and inflammation via cross talk of reactive oxygen and nitrogen species from mitochondria or nadph oxidase—implicatio…

2020

Oxidative stress plays a key role for the development of cardiovascular, metabolic, and neurodegenerative disease. This concept has been proven by using the approach of genetic deletion of reactive oxygen and nitrogen species (RONS) producing, pro-oxidant enzymes as well as by the overexpression of RONS detoxifying, antioxidant enzymes leading to an amelioration of the severity of diseases. Vice versa, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of RONS detoxifying enzymes. We have previously identified cross talk mechanisms between different sources of RONS, which can amplify the oxidative stress-m…

0301 basic medicineAntioxidantmedicine.medical_treatmentReview030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causelcsh:Chemistry0302 clinical medicineEndothelial dysfunctionEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyNADPH oxidasebiologyChemistryGeneral MedicineReactive Nitrogen SpeciesComputer Science ApplicationsCell biologyMitochondriaCardiovascular DiseasesDisease Progressionmedicine.symptomInflammationENOS uncouplingOxidative phosphorylationEndothelial dysfunction; ENOS uncoupling; Kindling radicals; Low-grade inflammation; Mitochondria; NADPH oxidase; Oxidative stress; Redox cross talkLow-grade inflammationCatalysisRedox cross talkInorganic Chemistry03 medical and health sciencesmedicineDiabetes MellitusAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInflammationNADPH oxidaseOrganic ChemistryNADPH Oxidasesmedicine.diseaseAngiotensin II030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oxidative stressbiology.proteinKindling radicalsReactive Oxygen SpeciesOxidative stress
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PPAR gamma agonist leriglitazone improves frataxin-loss impairments in cellular and animal models of Friedreich Ataxia

2020

Friedreich ataxia (FRDA), the most common autosomal recessive ataxia, is characterized by degeneration of the large sensory neurons and spinocerebellar tracts, cardiomyopathy, and increased incidence in diabetes. The underlying pathophysiological mechanism of FRDA, driven by a significantly decreased expression of frataxin (FXN), involves increased oxidative stress, reduced activity of enzymes containing iron‑sulfur clus-ters (ISC), defective energy production, calcium dyshomeostasis, and impaired mitochondrial biogenesis, leading to mitochondrial dysfunction. The peroxisome proliferator-activated receptor gamma (PPARγ) is a ligand-activated transcriptional factor playing a key role in mito…

0301 basic medicineAtaxiaCell SurvivalCaspase 3PPAR agonistlcsh:RC321-57103 medical and health sciencesMice0302 clinical medicineIron-Binding ProteinsmedicineNeuritesAnimalsHumansMyocytes CardiacNeurodegenerationDorsal root ganglia neuronslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMembrane Potential MitochondrialNeuronsCardiomyocytesbiologyChemistryFrataxinNeurodegenerationCalpainLipid DropletsPeroxisomemedicine.diseaseCell biologyMitochondriaRatsPPAR gamma030104 developmental biologyNeurologyMitochondrial biogenesisFriedreich AtaxiaFrataxinbiology.proteinThiazolidinedionesmedicine.symptomMitochondrial function030217 neurology & neurosurgery
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Friedreich Ataxia: current state-of-the-art, and future prospects for mitochondrial-focused therapies

2021

Friedreichs Ataxia is an autosomal recessive genetic disease causing the defective gene product, frataxin. A body of literature has been focused on the attempts to counteract frataxin deficiency and the consequent iron imbalance, in order to mitigate the disease-associated prooxidant state and clinical course. The present mini review is aimed at evaluating the basic and clinical reports on the roles and the use of a set of iron chelators, antioxidants and some cofactors involved in the key mitochondrial functions. Extensive literature has focused on the protective roles of iron chelators, coenzyme Q10 and analogs, and vitamin E, altogether with varying outcomes in clinical studies. Other st…

0301 basic medicineAtaxiaUbiquinoneAlpha-Lipoic AcidDiseaseMitochondrionIron Chelating AgentsBioinformaticsAntioxidantsLinoleic Acid03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCarnitinePhysiology (medical)AnimalsHumansMedicineDeferiproneCarnitineInner mitochondrial membraneCoenzyme Q10biologyAnimalbusiness.industryBiochemistry (medical)Public Health Environmental and Occupational HealthGeneral MedicineMitochondriaIron Chelating Agent030104 developmental biologyLinoleic AcidschemistryFriedreich Ataxia030220 oncology & carcinogenesisFrataxinbiology.proteinAntioxidantmedicine.symptombusinessHumanmedicine.drugTranslational Research
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