Search results for "Comprehensive Invited Review"

showing 5 items of 5 documents

Molecular Strategies for Targeting Antioxidants to Mitochondria: Therapeutic Implications

2015

Mitochondrial function and specifically its implication in cellular redox/oxidative balance is fundamental in controlling the life and death of cells, and has been implicated in a wide range of human pathologies. In this context, mitochondrial therapeutics, particularly those involving mitochondria-targeted antioxidants, have attracted increasing interest as potentially effective therapies for several human diseases. For the past 10 years, great progress has been made in the development and functional testing of molecules that specifically target mitochondria, and there has been special focus on compounds with antioxidant properties. In this review, we will discuss several such strategies, …

AntioxidantPhysiologyPlant AlkaloidsCellsAntioxidant propertiesmedicine.medical_treatmentClinical BiochemistryApoptosisContext (language use)Oxidative phosphorylationBiologyMitochondrionBiochemistryCellular redox/oxidative balanceAntioxidantsComprehensive Invited ReviewAutophagymedicineAnimalsHumansRedox activeMolecular BiologyGeneral Environmental ScienceHuman pathologiesAutophagyRedox active moleculesCell BiologyMitochondriaCell biologyBiochemistryGeneral Earth and Planetary SciencesMitochondrial functionTesting of moleculesOxidation-ReductionFunction (biology)Antioxidants & Redox Signaling
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Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities.

2011

Reactive oxygen species, such as superoxide and hydrogen peroxide, are generated in all cells by mitochondrial and enzymatic sources. Left unchecked, these reactive species can cause oxidative damage to DNA, proteins, and membrane lipids. Glutathione peroxidase-1 (GPx-1) is an intracellular antioxidant enzyme that enzymatically reduces hydrogen peroxide to water to limit its harmful effects. Certain reactive oxygen species, such as hydrogen peroxide, are also essential for growth factor-mediated signal transduction, mitochondrial function, and maintenance of normal thiol redox-balance. Thus, by limiting hydrogen peroxide accumulation, GPx-1 also modulates these processes. This review explor…

GPX1AntioxidantPhysiologyProtein Conformationmedicine.medical_treatmentClinical BiochemistryMolecular Sequence DataGene ExpressionBiologymedicine.disease_causeBiochemistryDiabetes mellitus geneticschemistry.chemical_compoundGlutathione Peroxidase GPX1Risk FactorsComprehensive Invited ReviewNeoplasmsmedicineDiabetes MellitusAnimalsHumansGenetic Predisposition to DiseaseAmino Acid SequenceEnzyme InhibitorsHydrogen peroxideMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasePolymorphism GeneticCell DeathSuperoxideCell BiologyGlutathioneSelenocysteineOxidative StresschemistryBiochemistryGene Expression RegulationCardiovascular DiseasesGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressAntioxidantsredox signaling
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Organic Nitrate Therapy, Nitrate Tolerance, and Nitrate-Induced Endothelial Dysfunction: Emphasis on Redox Biology and Oxidative Stress

2015

Abstract Organic nitrates, such as nitroglycerin (GTN), isosorbide-5-mononitrate and isosorbide dinitrate, and pentaerithrityl tetranitrate (PETN), when given acutely, have potent vasodilator effects improving symptoms in patients with acute and chronic congestive heart failure, stable coronary artery disease, acute coronary syndromes, or arterial hypertension. The mechanisms underlying vasodilation include the release of •NO or a related compound in response to intracellular bioactivation (for GTN, the mitochondrial aldehyde dehydrogenase [ALDH-2]) and activation of the enzyme, soluble guanylyl cyclase. Increasing cyclic guanosine-3′,-5′-monophosphate (cGMP) levels lead to an activation of…

Vascular smooth musclePhysiologyVasodilator AgentsClinical BiochemistryVasodilationPharmacologymedicine.disease_causeBiochemistryCalcium in biologyComprehensive Invited ReviewmedicineAnimalsHumansEndothelial dysfunctionMolecular BiologyGeneral Environmental ScienceNitratesChemistryCell Biologymedicine.diseaseOxidative StressCardiovascular DiseasesGeneral Earth and Planetary SciencesEndothelium VascularIsosorbide dinitrateReactive Oxygen SpeciesSoluble guanylyl cyclaseOxidation-ReductionOxidative stressIntracellularmedicine.drugAntioxidants & Redox Signaling
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The Adverse Effects of Environmental Noise Exposure on Oxidative Stress and Cardiovascular Risk

2018

Abstract Epidemiological studies have provided evidence that traffic noise exposure is linked to cardiovascular diseases such as arterial hypertension, myocardial infarction, and stroke. Noise is a nonspecific stressor that activates the autonomous nervous system and endocrine signaling. According to the noise reaction model introduced by Babisch and colleagues, chronic low levels of noise can cause so-called nonauditory effects, such as disturbances of activity, sleep, and communication, which can trigger a number of emotional responses, including annoyance and subsequent stress. Chronic stress in turn is associated with cardiovascular risk factors, comprising increased blood pressure and …

0301 basic medicinemedicine.medical_specialtyPhysiologyClinical Biochemistrytraffic noise exposure030204 cardiovascular system & hematologyenvironmental risk factorsmedicine.disease_causeBiochemistryendothelial dysfunctionCoronary artery disease03 medical and health sciences0302 clinical medicinestress hormonesComprehensive Invited ReviewRisk FactorsInternal medicineDiabetes mellitusmedicineHumansChronic stressMyocardial infarctionEndothelial dysfunctionMolecular BiologyStrokeGeneral Environmental Sciencebusiness.industryaircraft noise exposureEnvironmental ExposureCell Biologymedicine.diseaseStrokeOxidative Stress030104 developmental biologyBlood pressureCardiovascular DiseasesHypertensionCardiologyGeneral Earth and Planetary SciencesEnvironmental PollutantsNoiseReactive Oxygen SpeciesbusinessOxidative stressAntioxidants & Redox Signaling
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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