Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms

Forkhead box O class proteins (FoxOs) are expressed nearly in all tissues and are involved in different functions such as energy metabolism, redox homeostasis, differentiation, and cell cycle arrest. The plasticity of FoxOs is demonstrated by post-translational modifications that determine diverse l...

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Main Authors: Laura Ioannilli, Fabio Ciccarone, Maria Rosa Ciriolo
Format: Article
Language:English
Published: MDPI AG 2020-03-01
Series:Cells
Subjects:
Online Access:https://www.mdpi.com/2073-4409/9/4/849
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author Laura Ioannilli
Fabio Ciccarone
Maria Rosa Ciriolo
author_facet Laura Ioannilli
Fabio Ciccarone
Maria Rosa Ciriolo
author_sort Laura Ioannilli
collection DOAJ
description Forkhead box O class proteins (FoxOs) are expressed nearly in all tissues and are involved in different functions such as energy metabolism, redox homeostasis, differentiation, and cell cycle arrest. The plasticity of FoxOs is demonstrated by post-translational modifications that determine diverse levels of transcriptional regulations also controlled by their subcellular localization. Among the different members of the FoxO family, we will focus on FoxO1 in adipose tissue, where it is abundantly expressed and is involved in differentiation and transdifferentiation processes. The capability of FoxO1 to respond differently in dependence of adipose tissue subtype underlines the specific involvement of the transcription factor in energy metabolism and the “browning” process of adipocytes. FoxO1 can localize to nuclear, cytoplasm, and mitochondrial compartments of adipocytes responding to different availability of nutrients and source of reactive oxygen species (ROS). Specifically, fasted state produced-ROS enhance the nuclear activity of FoxO1, triggering the transcription of lipid catabolism and antioxidant response genes. The enhancement of lipid catabolism, in combination with ROS buffering, allows systemic energetic homeostasis and metabolic adaptation of white/beige adipocytes. On the contrary, a fed state induces FoxO1 to accumulate in the cytoplasm, but also in the mitochondria where it affects mitochondrial DNA gene expression. The importance of ROS-mediated signaling in FoxO1 subcellular localization and retrograde communication will be discussed, highlighting key aspects of FoxO1 multifaceted regulation in adipocytes.
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spelling doaj.art-3232a49e7cd94b8dbe78957b7a46546e2023-11-19T20:18:00ZengMDPI AGCells2073-44092020-03-019484910.3390/cells9040849Adipose Tissue and FoxO1: Bridging Physiology and MechanismsLaura Ioannilli0Fabio Ciccarone1Maria Rosa Ciriolo2Department of Biology, University of Rome “Tor Vergata”, Via della Ricerca Scientifica, 00133 Rome, ItalyIRCCS San Raffaele Pisana, Department of Human Sciences and Promotion of the Quality of Life, San Raffaele Roma Open University, Via di Val Cannuta 247, 00166 Rome, ItalyDepartment of Biology, University of Rome “Tor Vergata”, Via della Ricerca Scientifica, 00133 Rome, ItalyForkhead box O class proteins (FoxOs) are expressed nearly in all tissues and are involved in different functions such as energy metabolism, redox homeostasis, differentiation, and cell cycle arrest. The plasticity of FoxOs is demonstrated by post-translational modifications that determine diverse levels of transcriptional regulations also controlled by their subcellular localization. Among the different members of the FoxO family, we will focus on FoxO1 in adipose tissue, where it is abundantly expressed and is involved in differentiation and transdifferentiation processes. The capability of FoxO1 to respond differently in dependence of adipose tissue subtype underlines the specific involvement of the transcription factor in energy metabolism and the “browning” process of adipocytes. FoxO1 can localize to nuclear, cytoplasm, and mitochondrial compartments of adipocytes responding to different availability of nutrients and source of reactive oxygen species (ROS). Specifically, fasted state produced-ROS enhance the nuclear activity of FoxO1, triggering the transcription of lipid catabolism and antioxidant response genes. The enhancement of lipid catabolism, in combination with ROS buffering, allows systemic energetic homeostasis and metabolic adaptation of white/beige adipocytes. On the contrary, a fed state induces FoxO1 to accumulate in the cytoplasm, but also in the mitochondria where it affects mitochondrial DNA gene expression. The importance of ROS-mediated signaling in FoxO1 subcellular localization and retrograde communication will be discussed, highlighting key aspects of FoxO1 multifaceted regulation in adipocytes.https://www.mdpi.com/2073-4409/9/4/849ROSfasted stateadipogenesisbrowningmitochondria
spellingShingle Laura Ioannilli
Fabio Ciccarone
Maria Rosa Ciriolo
Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
Cells
ROS
fasted state
adipogenesis
browning
mitochondria
title Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
title_full Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
title_fullStr Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
title_full_unstemmed Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
title_short Adipose Tissue and FoxO1: Bridging Physiology and Mechanisms
title_sort adipose tissue and foxo1 bridging physiology and mechanisms
topic ROS
fasted state
adipogenesis
browning
mitochondria
url https://www.mdpi.com/2073-4409/9/4/849
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AT fabiociccarone adiposetissueandfoxo1bridgingphysiologyandmechanisms
AT mariarosaciriolo adiposetissueandfoxo1bridgingphysiologyandmechanisms