PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO
Peroxisome-proliferator activator receptor γ (PPARγ) is a nuclear receptor of central importance in energy homeostasis and inflammation. Recent experimental pieces of evidence demonstrate that PPARγ is implicated in the oxidative stress response, an imbalance between antithetic prooxidation and anti...
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Online Access: | http://dx.doi.org/10.1155/2012/641087 |
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doaj-f0121c5f96204fb5aeeccf3505af353d2020-11-25T00:52:20ZengHindawi LimitedPPAR Research1687-47571687-47652012-01-01201210.1155/2012/641087641087PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXOSimone Polvani0Mirko Tarocchi1Andrea Galli2Gastroenterology Unit, Department of Clinical Pathophysiology, University of Florence, Viale Pieraccini 6, 50139 Firenze, ItalyGastroenterology Unit, Department of Clinical Pathophysiology, University of Florence, Viale Pieraccini 6, 50139 Firenze, ItalyGastroenterology Unit, Department of Clinical Pathophysiology, University of Florence, Viale Pieraccini 6, 50139 Firenze, ItalyPeroxisome-proliferator activator receptor γ (PPARγ) is a nuclear receptor of central importance in energy homeostasis and inflammation. Recent experimental pieces of evidence demonstrate that PPARγ is implicated in the oxidative stress response, an imbalance between antithetic prooxidation and antioxidation forces that may lead the cell to apoptotic or necrotic death. In this delicate and intricate game of equilibrium, PPARγ stands out as a central player devoted to the quenching and containment of the damage and to foster cell survival. However, PPARγ does not act alone: indeed the nuclear receptor is at the point of interconnection of various pathways, such as the nuclear factor erythroid 2-related factor 2 (NRF2), Wnt/β-catenin, and forkhead box proteins O (FOXO) pathways. Here we reviewed the role of PPARγ in response to oxidative stress and its interaction with other signaling pathways implicated in this process, an interaction that emerged as a potential new therapeutic target for several oxidative-related diseases.http://dx.doi.org/10.1155/2012/641087 |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Simone Polvani Mirko Tarocchi Andrea Galli |
spellingShingle |
Simone Polvani Mirko Tarocchi Andrea Galli PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO PPAR Research |
author_facet |
Simone Polvani Mirko Tarocchi Andrea Galli |
author_sort |
Simone Polvani |
title |
PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO |
title_short |
PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO |
title_full |
PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO |
title_fullStr |
PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO |
title_full_unstemmed |
PPAR𝜸 and Oxidative Stress: Con(𝜷) Catenating NRF2 and FOXO |
title_sort |
ppar𝜸 and oxidative stress: con(𝜷) catenating nrf2 and foxo |
publisher |
Hindawi Limited |
series |
PPAR Research |
issn |
1687-4757 1687-4765 |
publishDate |
2012-01-01 |
description |
Peroxisome-proliferator activator receptor γ (PPARγ) is a nuclear receptor of central importance in energy homeostasis and inflammation. Recent experimental pieces of evidence demonstrate that PPARγ is implicated in the oxidative stress response, an imbalance between antithetic prooxidation and antioxidation forces that may lead the cell to apoptotic or necrotic death. In this delicate and intricate game of equilibrium, PPARγ stands out as a central player devoted to the quenching and containment of the damage and to foster cell survival. However, PPARγ does not act alone: indeed the nuclear receptor is at the point of interconnection of various pathways, such as the nuclear factor erythroid 2-related factor 2 (NRF2), Wnt/β-catenin, and forkhead box proteins O (FOXO) pathways. Here we reviewed the role of PPARγ in response to oxidative stress and its interaction with other signaling pathways implicated in this process, an interaction that emerged as a potential new therapeutic target for several oxidative-related diseases. |
url |
http://dx.doi.org/10.1155/2012/641087 |
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1725242875823783936 |