Fiche du document
2014
- doi: 10.1155/2014/618652
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/doi/10.1155/2014/618652
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/pmid/24734255
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/eissn/2314-6753
Ce document est lié à :
info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_DA5E3AC459F50
info:eu-repo/semantics/openAccess , Copying allowed only for non-profit organizations , https://serval.unil.ch/disclaimer
Sujets proches
Earnings Wage rates Wage-fund Departmental salaries Remuneration Pay Salaries Compensation Working class--Wages Superannuation Pension plans Compensation Retirement pensions Type 1 diabetes Brittle diabetes IDDM (Disease) Ketosis prone diabetes Diabetes mellitus Insulin-dependent diabetesCiter ce document
V. Plaisance et al., « Role of MicroRNAs in Islet Beta-Cell Compensation and Failure during Diabetes. », Serveur académique Lausannois, ID : 10.1155/2014/618652
Métriques
Partage / Export
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.