Search results for " Toll-like receptors"

showing 4 items of 4 documents

Diabetic microangiopathy: Pathogenetic insights and novel therapeutic approaches.

2017

Diabetic microangiopathy, including retinopathy, is characterized by abnormal growth and leakage of small blood vessels, resulting in local edema and functional impairment of the depending tissues. Mechanisms leading to the impairment of microcirculation in diabetes are multiple and still largely unclear. However, a dysregulated vascular regeneration appears to play a key role. In addition, oxidative and hyperosmolar stress, as well as the activation of inflammatory pathways triggered by advanced glycation end-products and toll-like receptors, have been recognized as key underlying events. Here, we review recent knowledge on cellular and molecular pathways of microvascular disease in diabet…

0301 basic medicineGlycation End Products AdvancedPhysiologyDiabetes retinopathyGlycation End ProductsDiseaseFibroblast growth factorHMGB1DiabeteMicrocirculationCapillary Permeability03 medical and health sciencesGlycationDiabetes mellitusmedicineSettore MED/05 - Patologia ClinicaAnimalsHumansCellular and molecular pathways; Diabetes; Diabetes retinopathy; Microangiopathy; Physiology; Molecular Medicine; PharmacologyNeovascularizationPharmacologyPathologicbiologyNeovascularization Pathologicbusiness.industryMicrocirculationMicroangiopathyDiabetesToll-Like Receptorsmedicine.diseasePrognosisCellular and molecular pathways; Diabetes; Diabetes retinopathy; Microangiopathy; Animals; Capillary Permeability; Diabetic Angiopathies; Glycation End Products Advanced; Humans; Inflammation Mediators; Microcirculation; Microvessels; Neovascularization Pathologic; Oxidative Stress; Prognosis; Signal Transduction; Toll-Like ReceptorsOxidative Stress030104 developmental biologyCellular and molecular pathwaysMicroangiopathyImmunologyMicrovesselsbiology.proteinMolecular MedicineAdvancedCellular and molecular pathwayInflammation MediatorsbusinessDiabetic AngiopathiesRetinopathySignal TransductionVascular pharmacology
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TLR4 expression in ex-Lichenoid lesions—oral squamous cell carcinomas and its surrounding epithelium: the role of tumor inflammatory microenvironment

2022

Toll-like receptors (TLRs) regulate innate and adaptive immune responses. Moreover, TLRs can induce a pro-survival and pro-proliferation response in tumor cells. This study aims to investigate the expression of TLR4 in the epithelium surrounding oral squamous cell carcinomas (OSCC) in relation to its inflammatory microenvironment. This study included 150 human samples: 30 normal oral control (NOC), 38 non-lichenoid epithelium surrounding OSCC (NLE-OSCC), 28 lichenoid epithelium surrounding OSCC (LE-OSCC), 30 OSCC ex-non oral lichenoid lesion (OSCC Ex-NOLL), and 24 OSCC ex-oral lichenoid lesion (OSCC Ex-OLL). TLR4 expression was investigated by immunohistochemistry and the percentage of posi…

InflammationSquamous Cell Carcinoma of Head and NeckNeoplasias bucaisBiochemistryReceptor 4 toll-likeEpitheliumToll-like receptorsToll-Like Receptor 4stomatognathic diseasestoll-like receptorsTumor microenvironmentinflammationMicroambiente tumoralHumanstoll-like receptortumor microenvironmentMouth Neoplasmshead and neck cancerTLR4Carcinoma de células escamosas de cabeça e pescoçohead and neck cancer; tumor microenvironment; inflammation; toll-like receptors; TLR4Head and neck cancerMolecular Biology
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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Pathogenetic Mechanisms of Hypertension-Brain-Induced Complications: Focus on Molecular Mediators.

2021

There is growing evidence that hypertension is the most important vascular risk factor for the development and progression of cardiovascular and cerebrovascular diseases. The brain is an early target of hypertension-induced organ damage and may manifest as stroke, subclinical cerebrovascular abnormalities and cognitive decline. The pathophysiological mechanisms of these harmful effects remain to be completely clarified. Hypertension is well known to alter the structure and function of cerebral blood vessels not only through its haemodynamics effects but also for its relationships with endothelial dysfunction, oxidative stress and inflammation. In the last several years, new possible mechani…

Settore MED/09 - Medicina InternaOrganic ChemistryToll-Like ReceptorsHemodynamicsBrainGeneral MedicineCatalysisCerebral complications Endothelial dysfunction Hypertension Innate immune system Neuroinflammation Oxidative stress Toll-like receptorsImmunity InnateComputer Science ApplicationsInorganic ChemistryOxidative StressHypertensionDisease ProgressionAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologySpectroscopyInternational journal of molecular sciences
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