Dicer1 deficient mice exhibit premature aging and metabolic perturbations in adipocytes.
Fiche publication
Date publication
octobre 2022
Journal
iScience
Auteurs
Membres identifiés du Cancéropôle Est :
Pr BAHRAM Siamak, Dr OREND Gertraud, Dr CARAPITO Raphaël
Tous les auteurs :
De Cauwer A, Loustau T, Erne W, Pichot A, Molitor A, Stemmelen T, Carapito R, Orend G, Bahram S, Georgel P
Lien Pubmed
Résumé
Age-related diseases are major concern in developed countries. To avoid disabilities that accompany increased lifespan, pharmaceutical approaches are considered. Therefore, appropriate animal models are required for a better understanding of aging processes and potential assays to evaluate the impact of molecules that may delay the occurrence of age-related diseases. Few mouse models exhibiting pathological aging exist, but currently, none of them reproducibly mimics human diseases like osteoporosis, cognitive dysfunctions or sarcopenia that can be seen in some, but not all, elders. Here, we describe the premature aging phenotypes of Dicer-deficient mature animals, which exhibit an overall deterioration of many organs and tissues (skin, heart, and adipose tissue) ultimately leading to a significant reduction of their lifespan. Molecular characterization of transcriptional responses focused on the adipose tissue suggested that both canonical and non-canonical functions of DICER are involved in this process and highlight potential actionable pathways to revert it.
Mots clés
Model organism, Molecular biology, Physiology
Référence
iScience. 2022 10 21;25(10):105149