MicroRNA-22 Is a Key Regulator of Lipid and Metabolic Homeostasis(67 views) Panella R, Petri A, Desai BN, Fagoonee S, Cotton CA, Nguyen PK, Lundin EM, Wagshal A, Wang DZ, Näär AM, Vlachos IS, Maratos-flier E, Altruda F, Kauppinen S, Paolo Pandolfi P
Int J Mol Sci (ISSN: 1422-0067linking), 2023 Aug 17; 24
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Center for Genomic Medicine, Desert Research Institute, Reno, NV 89512, USA.
Cancer Research Institute, Beth Israel Deaconess Cancer Center, Departments of Medicine and Pathology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA.
Center for RNA Medicine, Department of Clinical Medicine, Aalborg University, DK-2450 Copenhagen SV, Denmark.
Division of Endocrinology and Metabolism, Beth Israel Deaconess Medical Center, 330 Brookline Ave, Center for Life Sciences, Boston, MA 02215, USA.
Institute of Biostructure and Bioimaging (CNR) c/o Molecular Biotechnology Center, 10126 Turin, Italy.
Massachusetts General Hospital Cancer Center, Department of Cell Biology, Harvard Medical School, Boston, MA 02215, USA.
Boston Children's Hospital, Boston, MA 02215, USA.
Broad Institute of MIT and Harvard, Cambridge, MA 02142, USA.
Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Turin, 10126 Turin, Italy.
Renown Institute for Cancer, Nevada System of Higher Education, Reno, NV 89502, USA.
References: Not available.
MicroRNA-22 Is a Key Regulator of Lipid and Metabolic Homeostasis
Obesity is a growing public health problem associated with increased risk of type 2 diabetes, cardiovascular disease, nonalcoholic fatty liver disease (NAFLD) and cancer. Here, we identify microRNA-22 (miR-22) as an essential rheostat involved in the control of lipid and energy homeostasis as well as the onset and maintenance of obesity. We demonstrate through knockout and transgenic mouse models that miR-22 loss-of-function protects against obesity and hepatic steatosis, while its overexpression promotes both phenotypes even when mice are fed a regular chow diet. Mechanistically, we show that miR-22 controls multiple pathways related to lipid biogenesis and differentiation. Importantly, genetic ablation of miR-22 favors metabolic rewiring towards higher energy expenditure and browning of white adipose tissue, suggesting that modulation of miR-22 could represent a viable therapeutic strategy for treatment of obesity and other metabolic disorders.
MicroRNA-22 Is a Key Regulator of Lipid and Metabolic Homeostasis