Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes.

Détails

Ressource 1Télécharger: BIB_DA5E3AC459F5.P001.pdf (708.62 [Ko])
Etat: Serval
Version: de l'auteur
ID Serval
serval:BIB_DA5E3AC459F5
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes.
Périodique
Journal of Diabetes Research
Auteur(s)
Plaisance V., Waeber G., Regazzi R., Abderrahmani A.
ISSN
2314-6753 (Electronic)
Statut éditorial
Publié
Date de publication
2014
Peer-reviewed
Oui
Volume
2014
Pages
618652
Langue
anglais
Résumé
Pancreatic beta-cell function and mass are markedly adaptive to compensate for the changes in insulin requirement observed during several situations such as pregnancy, obesity, glucocorticoids excess, or administration. This requires a beta-cell compensation which is achieved through a gain of beta-cell mass and function. Elucidating the physiological mechanisms that promote functional beta-cell mass expansion and that protect cells against death, is a key therapeutic target for diabetes. In this respect, several recent studies have emphasized the instrumental role of microRNAs in the control of beta-cell function. MicroRNAs are negative regulators of gene expression, and are pivotal for the control of beta-cell proliferation, function, and survival. On the one hand, changes in specific microRNA levels have been associated with beta-cell compensation and are triggered by hormones or bioactive peptides that promote beta-cell survival and function. Conversely, modifications in the expression of other specific microRNAs contribute to beta-cell dysfunction and death elicited by diabetogenic factors including, cytokines, chronic hyperlipidemia, hyperglycemia, and oxidized LDL. This review underlines the importance of targeting the microRNA network for future innovative therapies aiming at preventing the beta-cell decline in diabetes.
Pubmed
Web of science
Open Access
Oui
Création de la notice
16/04/2014 16:33
Dernière modification de la notice
09/05/2019 2:04
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