0000000001215046

AUTHOR

Sebastiano Sciarretta

showing 10 related works from this author

Deregulation of TLR4 signaling pathway characterizes Bicuspid Aortic valve syndrome

2019

AbstractBicuspid aortic valve (BAV) disease is recognized to be a syndrome with a complex and multifaceted pathophysiology. Its progression is modulated by diverse evolutionary conserved pathways, such as Notch-1 pathway. Emerging evidence is also highlighting the key role of TLR4 signaling pathway in the aortic valve pathologies and their related complications, such as sporadic ascending aorta aneurysms (AAA). Consistent with these observations, we aimed to evaluate the role of TLR4 pathway in both BAV disease and its common complication, such as AAA. To this aim, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mea…

Male0301 basic medicineAortic valveBicuspid Aortic valve syndromeHeart Valve Diseaseslcsh:MedicineDisease0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseTLR4lcsh:ScienceAortaAged 80 and overMultidisciplinarySyndromeMiddle AgedPathophysiologymedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyFemaleSignal Transductionmedicine.medical_specialtyCardiologyArticleProinflammatory cytokine03 medical and health sciencesmedicine.arteryInternal medicineAscending aortamedicineHumansbicuspid valveAgedbicuspid valve; TLR4; aortic diseaseBAV TLR4 AAATumor Necrosis Factor-alphabusiness.industryInterleukinslcsh:RSettore MED/23 - Chirurgia CardiacaValvular diseaseaortic diseasemedicine.diseaseToll-Like Receptor 4030104 developmental biologyTLR4lcsh:QbusinessComplication030217 neurology & neurosurgeryScientific Reports
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Deregulation of Notch1 pathway and circulating endothelial progenitor cell (EPC) number in patients with bicuspid aortic valve with and without ascen…

2018

AbstractBicuspid aortic valve (BAV) is frequently associated with the development of ascending aortic aneurysm, even if the underlying mechanisms remain to be clarified. Here, we investigated if a deregulation of Notch1 signaling pathway and endothelial progenitor cells (EPCs) number is associated with BAV disease and an early ascending aortic aneurysm (AAA) onset. For this purpose, 70 subjects with BAV (M/F 50/20; mean age: 58.8 ± 14.8 years) and 70 subjects with tricuspid aortic valve (TAV) (M/F 35/35; mean age: 69.1 ± 12.8 years) and AAA complicated or not, were included. Interestingly, patients with AAA showed a significant increase in circulating Notch1 levels and EPC number than subje…

Male0301 basic medicineAortic valveNotch1 signaling pathwatHeart Valve Diseases030204 cardiovascular system & hematologyAortic aneurysm0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseNotch Signaling Pathwaycirculating EPC populationsReceptor Notch1ReceptorAortaEndothelial Progenitor CellsAged 80 and overMultidisciplinaryQRMiddle AgedAortic Aneurysmmedicine.anatomical_structureAortic Valvecardiovascular systemCardiologyMedicineFemaleTricuspid ValveSignal TransductionAdultmedicine.medical_specialtyBicuspid aortic valveEndothelial Progenitor Cells (EPC)ScienceNotch signaling pathwayBicuspid Aortic Valve (BAV)Endothelial progenitor cellArticleBicuspid aortic valve; Notch1 signaling pathwat; ascending aortic aneurysm03 medical and health sciencesascending aortic aneurysmInternal medicinemedicineHumansIn patientcardiovascular diseasesProgenitor cellNotch 1 signaling pathwayAgedTricuspid Aortic Valve (TAV)Ascending Aorta Aneurysm (AAA)business.industrySettore MED/23 - Chirurgia Cardiacamedicine.disease030104 developmental biologybusiness
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Targeting Nitric Oxide with Natural Derived Compounds as a Therapeutic Strategy in Vascular Diseases

2016

Within the family of endogenous gasotransmitters, nitric oxide (NO) is the smallest gaseous intercellular messenger involved in the modulation of several processes, such as blood flow and platelet aggregation control, essential to maintain vascular homeostasis. NO is produced by nitric oxide synthases (NOS) and its effects are mediated by cGMP-dependent or cGMP-independent mechanisms. Growing evidence suggests a crosstalk between the NO signaling and the occurrence of oxidative stress in the onset and progression of vascular diseases, such as hypertension, heart failure, ischemia, and stroke. For these reasons, NO is considered as an emerging molecular target for developing therapeutic stra…

0301 basic medicineAgingPhytochemicalsIschemiaEndogenyReview Article030204 cardiovascular system & hematologyPharmacologyBiologyNitric Oxidemedicine.disease_causeCardiovascular SystemBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineAnimalsHumansVascular Diseasescell biology; aging; biochemistrylcsh:QH573-671GasotransmittersPlants Medicinallcsh:CytologyPolyphenolsCardiovascular AgentsCell BiologyGeneral Medicinemedicine.diseaseDietOxidative StressCrosstalk (biology)030104 developmental biologychemistryHeart failurePlant PreparationsOxidative stressIntracellularPhytotherapySignal TransductionOxidative Medicine and Cellular Longevity
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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

2016

Seuls les 100 premiers auteurs dont les auteurs INRA ont été entrés dans la notice. La liste complète des auteurs et de leurs affiliations est accessible sur la publication.; International audience; In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues…

[SDV]Life Sciences [q-bio]autophagosomeReview Articleddc:616.07stressstreLC3MESH: AnimalsSettore MED/49 - Scienze Tecniche Dietetiche ApplicateSettore BIO/06 - Anatomia Comparata E Citologiachaperone-mediated autophagyComputingMilieux_MISCELLANEOUSSettore BIO/11Pharmacology. TherapySettore BIO/13standards [Biological Assay]autolysosomeMESH: Autophagy*/physiologylysosomemethods [Biological Assay]Biological AssaySettore BIO/17 - ISTOLOGIAErratumHumanBiochemistry & Molecular BiologySettore BIO/06physiology [Autophagy]Chaperonemediated autophagy[SDV.BC]Life Sciences [q-bio]/Cellular BiologyNOautophagy guidelines molecular biology ultrastructureautolysosome; autophagosome; chaperone-mediated autophagy; flux; LC3; lysosome; macroautophagy; phagophore; stress; vacuoleMESH: Biological Assay/methodsMESH: Computer Simulationddc:570Autolysosome Autophagosome Chaperonemediated autophagy Flux LC3 Lysosome Macroautophagy Phagophore Stress VacuoleAutophagyAnimalsHumansComputer SimulationSettore BIO/10ddc:612BiologyphagophoreMESH: HumansvacuoleAnimalLC3; autolysosome; autophagosome; chaperone-mediated autophagy; flux; lysosome; macroautophagy; phagophore; stress; vacuole; Animals; Biological Assay; Computer Simulation; Humans; Autophagy0601 Biochemistry And Cell BiologyfluxmacroautophagyMESH: Biological Assay/standards*Human medicineLC3; autolysosome; autophagosome; chaperone-mediated autophagy; flux; lysosome; macroautophagy; phagophore; stress; vacuole
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A Typical Immune T/B Subset Profile Characterizes Bicuspid Aortic Valve: In an Old Status?

2018

Bicuspid valve disease is associated with the development of thoracic aortic aneurysm. The molecular mechanisms underlying this association still need to be clarified. Here, we evaluated the circulating levels of T and B lymphocyte subsets associated with the development of vascular diseases in patients with bicuspid aortic valve or tricuspid aortic valve with and without thoracic aortic aneurysm. We unveiled that the circulating levels of the MAIT, CD4+IL−17A+, and NKT T cell subsets were significantly reduced in bicuspid valve disease cases, when compared to tricuspid aortic valve cases in either the presence or the absence of thoracic aortic aneurysm. Among patients with tricuspid aortic…

Male0301 basic medicineAortic valveAgingT-LymphocytesLymphocyteHeart Valve Diseases030204 cardiovascular system & hematologyBiochemistryImmunoglobulin D0302 clinical medicineBicuspid aortic valveBicuspid Aortic Valve DiseaseBicuspid aortic valve aneurysm B cellsb-cellsnotch1Invariant t-cells; aneurysm formation; angiotensin-ii; signaling pathway; genetic-variants; apoptotic cells; b-cells; mechanisms; mutations; notch1B-Lymphocytesmechanismsbiologylcsh:Cytologyhemic and immune systemsGeneral MedicineMiddle Agedmedicine.anatomical_structureAortic ValveCardiologycardiovascular systemFemaleResearch Articlesignaling pathwaymedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesaneurysm formationInvariant t-cellsArticle SubjectBicuspid aortic valveT cellNaive B cellchemical and pharmacologic phenomenaThoracic aortic aneurysm03 medical and health sciencesBicuspid valveInternal medicinemedicineHumansSettore MED/05 - Patologia Clinicacardiovascular diseaseslcsh:QH573-671angiotensin-iigenetic-variantsB cellsbusiness.industrySettore MED/23 - Chirurgia Cardiacaapoptotic cellsCell Biologymutationsmedicine.disease030104 developmental biologybiology.proteinaneurysmbusinessA Typical Immune T/B Subset Profile Bicuspid Aortic Valve
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An overview of the molecular mechanisms underlying development and progression of bicuspid aortic valve disease

2019

Bicuspid aortic valve (BAV) is a common congenital heart malformation frequently associated with the development of aortic valve diseases and severe aortopathy, such as aortic dilatation, aneurysm and dissection. To date, different genetic loci have been identified in syndromic and non- syndromic forms of BAV. Among these, genes involved in the regulation of extracellular matrix remodelling, epithelial to mesenchymal transition and nitric oxide metabolism appear to be the main contributors to BAV pathogenesis. However, no- single gene model explains BAV inheritance, suggesting that more factors are simultaneously involved. In this regard, characteristic epigenetic and immunological profiles…

0301 basic medicineaneurysm; aortic dilatation; aortic stenosis; aortopathy; bicuspid aortic valve; NOTCH1Aortic stenosibicuspid aortic valveHeart malformationAortic DiseasesHeart Valve Diseasesaortopathy610 Medicine & healthDisease030204 cardiovascular system & hematologyBioinformatics2705 Cardiology and Cardiovascular Medicine11459 Center for Molecular CardiologyPathogenesis03 medical and health sciences0302 clinical medicineAneurysmBicuspid aortic valveNOTCH1Bicuspid Aortic Valve Disease1312 Molecular BiologymedicineSettore MED/05 - Patologia ClinicaAnimalsHumansEpithelial–mesenchymal transitionEpigeneticsMolecular BiologyAortic dilatationbusiness.industryaortic stenosisaortic dilatationmedicine.disease030104 developmental biologyAortic ValveaneurysmDisease Progressioncardiovascular systemCardiology and Cardiovascular MedicinebusinessJournal of Molecular and Cellular Cardiology
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Light on the molecular and cellular mechanisms of bicuspid aortic valve to unveil phenotypic heterogeneity

2019

Research on bicuspid aortic valve disease (BAV) and related complications has grown in an exponential manner in the last decades. However, the current knowledge of the mechanisms underlying the development of this disease is still limited, since all clinical and surgical studies on BAV mainly focused their objects on its major vascular complications, such as ascending aortic aneurysms and dissection. It is now clear that a better understanding of the pivotal molecular and cellular pathophysiological aspects of bicuspid valve aortopathy, including natural history, phenotypic expression, histology, cellular mechanisms and pathways, is critical for improving its clinical management. This chang…

molecular and cellular mechanismbicuspid aortic valvethoracicphenotypeprecision medicineaortic aneurysm thoracic; aortic valve; biomarkers; heart valve diseases; humans; precision medicine; genetic heterogeneity; phenotypeBiologyBioinformaticsheart valve diseasesgenetic heterogeneityAortic aneurysmBicuspid aortic valveBicuspid Aortic Valve DiseasemedicineSettore MED/05 - Patologia ClinicahumansMolecular BiologyAortic Aneurysm ThoracicGenetic heterogeneitybiomarkersmedicine.diseasePrecision medicineaortic valvePhenotypeCardiology and Cardiovascular Medicineaortic aneurysmJournal of Molecular and Cellular Cardiology
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Erratum

2016

Author(s): Klionsky, DJ; Abdelmohsen, K; Abe, A; Abedin, MJ; Abeliovich, H; Arozena, AA; Adachi, H; Adams, CM; Adams, PD; Adeli, K; Adhihetty, PJ; Adler, SG; Agam, G; Agarwal, R; Aghi, MK; Agnello, M; Agostinis, P; Aguilar, PV; Aguirre-Ghiso, J; Airoldi, EM; Ait-Si-Ali, S; Akematsu, T; Akporiaye, ET; Al-Rubeai, M; Albaiceta, GM; Albanese, C; Albani, D; Albert, ML; Aldudo, J; Algul, H; Alirezaei, M; Alloza, I; Almasan, A; Almonte-Beceril, M; Alnemri, ES; Alonso, C; Altan-Bonnet, N; Altieri, DC; Alvarez, S; Alvarez-Erviti, L; Alves, S; Amadoro, G; Amano, A; Amantini, C; Ambrosio, S; Amelio, I; Amer, AO; Amessou, M; Amon, A; An, Z; Anania, FA; Andersen, SU; Andley, UP; Andreadi, CK; Andrieu-Ab…

0301 basic medicineSettore BIO/06biologyCell Biology[SDV.BC]Life Sciences [q-bio]/Cellular Biologybiology.organism_classificationCell biologyInterpretation (model theory)03 medical and health sciencesArama030104 developmental biologyMolecular BiologyHumanitiesComputingMilieux_MISCELLANEOUS
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Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

2021

Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to…

0301 basic medicineProgrammed cell deathSettore BIO/06AutophagosomeAutolysosome[SDV]Life Sciences [q-bio]lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4]Autophagy-Related ProteinsReviewComputational biology[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologySettore MED/0403 medical and health sciencesstressChaperone-mediated autophagyddc:570AutophagyLC3AnimalsHumanscancerSettore BIO/10Autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSet (psychology)Molecular Biologyvacuole.phagophore030102 biochemistry & molecular biologyvacuolebusiness.industryInterpretation (philosophy)AutophagyAutophagosomesneurodegenerationCell BiologyfluxMulticellular organismmacroautophagy030104 developmental biologyKnowledge baselysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleBiological AssayLysosomesbusinessBiomarkers[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Autophagy

2021

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide…

macroautophagy;autophagyAutophagosome[SDV]Life Sciences [q-bio]canceLC3 macroautophagyautophagosomeneurodegeneration;[SDV.BC]Life Sciences [q-bio]/Cellular BiologyAutophagy AutophagosomeNOstress vacuolestressautophagic processesstrerfluxLC3cancerguidelinesAutophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/06 - Anatomia Comparata E Citologia[SDV.BC] Life Sciences [q-bio]/Cellular BiologyComputingMilieux_MISCELLANEOUSMedaka oryzias latipesphagophorevacuoleQHneurodegenerationAutophagosome cancer flux LC3 lysosome macroautophagy neurodegeneration phagophore stress vacuoleautophagy; autophagic processes; guidelines; autophagosome; cancer; flux; LC3; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuolefluxmacroautophagystress.lysosomeAutophagosome; LC3; cancer; flux; lysosome; macroautophagy; neurodegeneration; phagophore; stress; vacuoleSettore BIO/17 - ISTOLOGIARC
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