Targeting hIAPP fibrillation: A new paradigm to prevent β-cell death?
| dc.rights.license | open | en_US |
| dc.contributor.author | GUILLEMAIN, Ghislaine | |
| dc.contributor.author | LACAPERE, Jean-Jacques | |
| hal.structure.identifier | Chimie et Biologie des Membranes et des Nanoobjets [CBMN] | |
| dc.contributor.author | KHEMTEMOURIAN, Lucie | |
| dc.date.accessioned | 2023-04-18T08:58:51Z | |
| dc.date.available | 2023-04-18T08:58:51Z | |
| dc.date.issued | 2022-10-01 | |
| dc.identifier.issn | 0005-2736 | en_US |
| dc.identifier.uri | https://oskar-bordeaux.fr/handle/20.500.12278/173049 | |
| dc.description.abstractEn | Loss 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.iso | EN | en_US |
| dc.subject.en | Type 2 diabetes | |
| dc.subject.en | Pancreas | |
| dc.subject.en | β-cells | |
| dc.subject.en | Cross-fibrils | |
| dc.subject.en | Amyloid proteins | |
| dc.title.en | Targeting hIAPP fibrillation: A new paradigm to prevent β-cell death? | |
| dc.title.alternative | Biochimica et Biophysica Acta (BBA) - Biomembranes | en_US |
| dc.type | Article de revue | en_US |
| dc.identifier.doi | 10.1016/j.bbamem.2022.184002 | en_US |
| dc.subject.hal | Chimie/Matériaux | en_US |
| bordeaux.journal | Biochimica et Biophysica Acta (BBA) - Biomembranes | en_US |
| bordeaux.volume | 1864 | en_US |
| bordeaux.hal.laboratories | CBMN : Chimie & de Biologie des Membranes & des Nano-objets - UMR 5248 | en_US |
| bordeaux.issue | 10 | en_US |
| bordeaux.institution | Université de Bordeaux | en_US |
| bordeaux.institution | Bordeaux INP | en_US |
| bordeaux.institution | CNRS | en_US |
| bordeaux.peerReviewed | oui | en_US |
| bordeaux.inpress | non | en_US |
| hal.export | false | |
| dc.rights.cc | Pas de Licence CC | en_US |
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