Mostrar el registro sencillo del ítem

dc.rights.licenseopenen_US
dc.contributor.authorGUILLEMAIN, Ghislaine
dc.contributor.authorLACAPERE, Jean-Jacques
hal.structure.identifierChimie et Biologie des Membranes et des Nanoobjets [CBMN]
dc.contributor.authorKHEMTEMOURIAN, Lucie
dc.date.accessioned2023-04-18T08:58:51Z
dc.date.available2023-04-18T08:58:51Z
dc.date.issued2022-10-01
dc.identifier.issn0005-2736en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/173049
dc.description.abstractEnLoss of pancreatic β-cell mass is deleterious for type 2 diabetes patients since it reduces insulin production, critical for glucose homeostasis. The main research axis developed over the last few years was to generate new pancreatic β-cells or to transplant pancreatic islets as occurring for some specific type 1 diabetes patients. We evaluate here a new paradigm consisting in preservation of β-cells by prevention of human islet amyloid polypeptide (hIAPP) oligomers and fibrils formation leading to pancreatic β-cell death. We review the hIAPP physiology and the pathology that contributes to β-cell destruction, deciphering the various cellular steps that could be involved. Recent progress in understanding other amyloidosis such as Aβ, Tau, α-synuclein or prion, involved in neurodegenerative processes linked with inflammation, has opened new research lines of investigations to preserve neuronal cells. We evaluate and estimate their transposition to the pancreatic β-cells preservation. Among them is the control of reactive oxygen species (ROS) production occurring with inflammation and the possible implication of the mitochondrial translocator protein as a diagnostic and therapeutic target. The present review also focuses on other amyloid forming proteins from molecular to physiological and physiopathological points of view that could help to better decipher hIAPP-induced β-cell death mechanisms and to prevent hIAPP fibril formation.
dc.language.isoENen_US
dc.subject.enType 2 diabetes
dc.subject.enPancreas
dc.subject.enβ-cells
dc.subject.enCross-fibrils
dc.subject.enAmyloid proteins
dc.title.enTargeting hIAPP fibrillation: A new paradigm to prevent β-cell death?
dc.title.alternativeBiochimica et Biophysica Acta (BBA) - Biomembranesen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1016/j.bbamem.2022.184002en_US
dc.subject.halChimie/Matériauxen_US
bordeaux.journalBiochimica et Biophysica Acta (BBA) - Biomembranesen_US
bordeaux.volume1864en_US
bordeaux.hal.laboratoriesCBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248en_US
bordeaux.issue10en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionBordeaux INPen_US
bordeaux.institutionCNRSen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Biochimica%20et%20Biophysica%20Acta%20(BBA)%20-%20Biomembranes&rft.date=2022-10-01&rft.volume=1864&rft.issue=10&rft.eissn=0005-2736&rft.issn=0005-2736&rft.au=GUILLEMAIN,%20Ghislaine&LACAPERE,%20Jean-Jacques&KHEMTEMOURIAN,%20Lucie&rft.genre=article


Archivos en el ítem

Thumbnail

Este ítem aparece en la(s) siguiente(s) colección(ones)

Mostrar el registro sencillo del ítem