Search results for "Mito"

showing 10 items of 2513 documents

Oxidative stress modulates rearrangement of endoplasmic reticulum-mitochondria contacts and calcium dysregulation in a Friedreich's ataxia model

2020

Friedreich ataxia (FRDA) is a neurodegenerative disorder characterized by neuromuscular and neurological manifestations. It is caused by mutations in the FXN gene, which results in loss of the mitochondrial protein frataxin. Endoplasmic Reticulum-mitochondria associated membranes (MAMs) are inter-organelle structures involved in the regulation of essential cellular processes, including lipid metabolism and calcium signaling. In the present study, we have analyzed in both, unicellular and multicellular models of FRDA, calcium management and integrity of MAMs. We observed that function of MAMs is compromised in our cellular model of FRDA, which was improved upon treatment with antioxidants. I…

0301 basic medicineAtaxiaClinical BiochemistryLipid peroxidationchemistry.chemical_elementMitochondrionCalciumEndoplasmic ReticulumBiochemistry03 medical and health sciences0302 clinical medicineMAMsmedicineAnimalsVitamin EMitochondrial calcium uptakelcsh:QH301-705.5Calcium signalinglcsh:R5-920biologyFrataxinEndoplasmic reticulumOrganic ChemistryN-acetylcysteineMitochondriaCell biologyOxidative StressDrosophila melanogaster030104 developmental biologychemistrylcsh:Biology (General)Friedreich AtaxiaFrataxinbiology.proteinCalciummedicine.symptomCellular modellcsh:Medicine (General)030217 neurology & neurosurgeryResearch PaperRedox Biology
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Reversible Axonal Dystrophy by Calcium Modulation in Frataxin-Deficient Sensory Neurons of YG8R Mice

2017

15 Pages, 8 Figures. The Supplementary Material for this article can be found online at: http://journal.frontiersin.org/article/10.3389/fnmol.2017.00264/full#supplementary-material

0301 basic medicineAtaxiaNeuriteFriedreich’s ataxiarare diseaseMitochondrionlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neurosciencechemistry.chemical_compound0302 clinical medicineBAPTAmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchcalciumbiologyNeurodegenerationneurodegenerationFriedreich's ataxiaaxonal spheroidsmedicine.disease3. Good healthmitochondria030104 developmental biologyPeripheral neuropathychemistrynervous systemFrataxinbiology.proteinAxoplasmic transportmedicine.symptomNeuroscience030217 neurology & neurosurgeryNeuroscience
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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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Mitochondrial bioenergetic pathways in blood leukocyte transcriptome decrease after intensive weight loss but are rescued following weight regain in …

2021

Prolonged periods of energy deficit leading to weight loss induce metabolic adaptations resulting in reduced energy expenditure, but the mechanisms for energy conservation are incompletely understood. We examined 42 healthy athletic females (age 27.5 +/- 4.0 years, body mass index 23.4 +/- 1.7 kg/m(2)) who volunteered into either a group dieting for physique competition (n = 25) or a control group (n = 17). The diet group substantially reduced their energy intake and moderately increased exercise levels to induce loss of fat mass that was regained during a voluntary weight regain period. The control group maintained their typical lifestyle habits and body mass as instructed. From the diet g…

0301 basic medicineBioenergeticsWeight GainruokavaliotBiochemistryTranscriptomeravitsemuskäyttäytyminen0302 clinical medicineWeight lossaineenvaihdunta2. Zero hungerexerciseAdaptation PhysiologicalMitochondriaFemalemedicine.symptomenergiankulutus (aineenvaihdunta)fyysinen aktiivisuusBiotechnologyDietingAdultmedicine.medical_specialtyleukocytesmitokondriotoxidative phosphorylationBiologypainonnousuribosomesYoung Adult03 medical and health sciencesInternal medicineWeight LossGeneticsmedicineMetabolomeHumansMolecular Biologyitsensä johtaminenlaihdutusAMPKMetabolism030104 developmental biologyEndocrinologyenergiansaanti1182 Biochemistry cell and molecular biologylihavuus3111 BiomedicineEnergy IntakeTranscriptomedietBody mass index030217 neurology & neurosurgery
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Cardiolipin synthesis in brown and beige fat mitochondria is essential for systemic energy homeostasis

2018

Summary Activation of energy expenditure in thermogenic fat is a promising strategy to improve metabolic health, yet the dynamic processes that evoke this response are poorly understood. Here we show that synthesis of the mitochondrial phospholipid cardiolipin is indispensable for stimulating and sustaining thermogenic fat function. Cardiolipin biosynthesis is robustly induced in brown and beige adipose upon cold exposure. Mimicking this response through overexpression of cardiolipin synthase (Crls1) enhances energy consumption in mouse and human adipocytes. Crls1 deficiency in thermogenic adipocytes diminishes inducible mitochondrial uncoupling and elicits a nuclear transcriptional respons…

0301 basic medicineBiologiaBioenergeticsChop-10 ; Crls1 ; Beige Adipose ; Brown Adipose ; Cardiolipin ; Insulin Resistance ; Lipid Metabolism ; Mitochondria ; Phospholipids ; ThermogenesisPhysiologyGlucose uptakeAdipose tissueTransferases (Other Substituted Phosphate Groups)MitochondrionEnergy homeostasischemistry.chemical_compoundMice0302 clinical medicineAdipose Tissue Browninsulin resistancelipid metabolismCardiolipinAdipocytesCells CulturedThermogenesisthermogenesisCell biologyMitochondriamitochondriaCHOP-10lipids (amino acids peptides and proteins)BioquímicaCardiolipinsbeige adiposeArticle03 medical and health sciencesInsulin resistanceCRLS1medicineAnimalsHumansMolecular Biologyphospholipidsbrown adiposeMembrane ProteinsCell BiologyAdipose Tissue Beigemedicine.diseaseMice Inbred C57BL030104 developmental biologychemistrycardiolipinEnergy MetabolismThermogenesis030217 neurology & neurosurgery
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Polyphosphate as a metabolic fuel in Metazoa: A foundational breakthrough invention for biomedical applications

2015

In animals, energy-rich molecules like ATP are generated in the intracellular compartment from metabolites, e.g. glucose, taken up by the cells. Recent results revealed that inorganic polyphosphates (polyP) can provide an extracellular system for energy transport and delivery. These polymers of multiple phosphate units, linked by high-energy phosphoanhydride bonds, use blood platelets as transport vehicles to reach their target cells. In this review it is outlined how polyP affects cell metabolism. It is discussed that polyP influences cell activity in a dual way: (i) as a metabolic fuel transferring metabolic energy through the extracellular space; and (ii) as a signaling molecule that amp…

0301 basic medicineBiomedical TechnologyMitochondrionBiologyEndocytosisApplied Microbiology and Biotechnology03 medical and health scienceschemistry.chemical_compoundAdenosine TriphosphateTissue engineeringPolyphosphatesExtracellularHumansBlood CellsPolyphosphateGeneral MedicineCell biologyMitochondriaMetabolic pathway030104 developmental biologychemistryBiochemistryMolecular MedicineNanoparticlesAdenosine triphosphateIntracellularMetabolic Networks and PathwaysBiotechnology Journal
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Curcumin as a therapeutic option in retinal diseases

2020

Este artículo se encuentra disponible en la siguiente URL: https://www.mdpi.com/2076-3921/9/1/48 Este artículo pertenece al número especial "Natural products in health promotion and disease prevention". En este artículo también participa: Vincent M. Villar. The retina is subjected to oxidative stress due to its high vascularization, long time light exposition and a high density of mitochondria. Oxidative stress can lead to pathological processes, like cell apoptosis, angiogenesis and inflammation ending in retinal pathologies. Curcumin, a major bioactive component obtained from the spice turmeric (Curcuma longa) rhizome has been used for centuries in Asian countries for cooking and for curi…

0301 basic medicineBioquímicaretinaAntioxidantPhysiologyBioquímica clínicamedicine.medical_treatmentClinical BiochemistryCurcumina - Uso terapéutico.InflammationReviewPharmacologyMitochondrionmedicine.disease_causeBiochemistryRetina03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineoxidative stresscurcuminCurcumaMolecular BiologyVistachemistry.chemical_classificationEstrés oxidativo.Reactive oxygen speciesBiología molecularbiologybusiness.industryRetina - Diseases - Treatment.lcsh:RM1-950RetinalCell Biologybiology.organism_classificationCurcumin - Therapeutic use.Oxidative stress.030104 developmental biologylcsh:Therapeutics. Pharmacologyretinal diseaseschemistry030220 oncology & carcinogenesisCurcuminmedicine.symptombusinessCúrcumaOxidative stressRetina - Enfermedades - Tratamiento.
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Fine-Tuning of Platelet Responses by Serine/Threonine Protein Kinases and Phosphatases-Just the Beginning.

2021

AbstractComprehensive proteomic analyses of human and murine platelets established an extraordinary intracellular repertoire of signaling components, which control crucial functions. The spectrum of platelet serine/threonine protein kinases (more than 100) includes the AGC family (protein kinase A, G, C [PKA, PKG, PKC]), the mitogen-activated protein kinases (MAPKs), and others. PKA and PKG have multiple significantly overlapping substrates in human platelets, which possibly affect functions with clear “signaling nodes” of regulation by multiple protein kinases/phosphatases. Signaling nodes are intracellular Ca2+ stores, the contractile system (myosin light chains), and other signaling comp…

0301 basic medicineBlood PlateletsProteomicsThreonineMyosin Light ChainsPhosphataseSerine threonine protein kinase030204 cardiovascular system & hematology03 medical and health sciencesMice0302 clinical medicinePhosphoprotein PhosphatasesSerineAnimalsHumansSyk KinasePlatelet activationProtein kinase AProtein kinase CKinaseChemistryHematologyProtein phosphatase 2Platelet ActivationCell biology030104 developmental biologyModels AnimalMitogen-Activated Protein KinasesTyrosine kinaseProtein KinasesSignal TransductionHamostaseologie
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Sphingolipids and Inositol Phosphates Regulate the Tau Protein Phosphorylation Status in Humanized Yeast

2020

Hyperphosphorylation of protein tau is a hallmark of Alzheimer’s disease (AD). Changes in energy and lipid metabolism have been correlated with the late onset of this neurological disorder. However, it is uncertain if metabolic dysregulation is a consequence of AD or one of the initiating factors of AD pathophysiology. Also, it is unclear whether variations in lipid metabolism regulate the phosphorylation state of tau. Here, we show that in humanized yeast, tau hyperphosphorylation is stimulated by glucose starvation in coincidence with the downregulation of Pho85, the yeast ortholog of CDK5. Changes in inositol phosphate (IP) signaling, which has a central role in energy metabolism, altere…

0301 basic medicineCDK5Cèl·lulesTau proteinSit42HyperphosphorylationSaccharomyces cerevisiaeSACCHAROMYCES-CEREVISIAECeramide03 medical and health scienceschemistry.chemical_compoundCell and Developmental Biology0302 clinical medicineInositolceramideYpk1Inositol phosphatelcsh:QH301-705.51-IP7Original Researchchemistry.chemical_classificationScience & TechnologybiologyChemistryKinaseNEURODEGENERATIONLipid metabolismCell BiologyProtein phosphatase 2Fpk1MICROTUBULE-BINDINGPho85SERINE PALMITOYLTRANSFERASECell biologyALZHEIMERS-DISEASE030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisGLYCOGEN-SYNTHASE KINASE-3-BETAbiology.proteinKINASE-ACTIVITYPhosphorylationLife Sciences & BiomedicineBETA TOXICITYProteïnesDevelopmental BiologyFrontiers in Cell and Developmental Biology
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IL4 Primes the Dynamics of Breast Cancer Progression via DUSP4 Inhibition

2017

Abstract The tumor microenvironment supplies proinflammatory cytokines favoring a permissive milieu for cancer cell growth and invasive behavior. Here we show how breast cancer progression is facilitated by IL4 secreted by adipose tissue and estrogen receptor–positive and triple-negative breast cancer cell types. Blocking autocrine and paracrine IL4 signaling with the IL4Rα antagonist IL4DM compromised breast cancer cell proliferation, invasion, and tumor growth by downregulating MAPK pathway activity. IL4DM reduced numbers of CD44+/CD24− cancer stem-like cells and elevated expression of the dual specificity phosphatase DUSP4 by inhibiting NF-κB. Enforced expression of DUSP4 drove conversio…

0301 basic medicineCancer ResearchBlotting WesternCA 15-3Breast Neoplasms03 medical and health sciencesParacrine signalling0302 clinical medicineBreast cancerCell Line TumorTumor MicroenvironmentmedicineHumansskin and connective tissue diseasesAutocrine signallingDual-Specificity PhosphataseBlotting Western; Breast Neoplasms; Cell Line Tumor; Disease Progression; Dual-Specificity Phosphatases; Female; Flow Cytometry; Heterografts; Humans; Interleukin-4; Mitogen-Activated Protein Kinase Phosphatases; Tumor Microenvironment; Oncology; Cancer ResearchTumor microenvironmentbiologyCD44CancerFlow Cytometrymedicine.disease030104 developmental biologyOncology030220 oncology & carcinogenesisImmunologyCancer cellDisease Progressionbiology.proteinCancer researchDual-Specificity PhosphatasesHeterograftsMitogen-Activated Protein Kinase PhosphatasesFemaleInterleukin-4HeterograftMitogen-Activated Protein Kinase PhosphataseBreast NeoplasmHumanCancer Research
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