Journal ArticleDOI
The hormetic dose-response mechanism: Nrf2 activation
TLDR
A generalized mechanism for hormetic dose responses is proposed that is based on the redox-activated transcription factor (TF), Nrf2, and its upregulation of an integrative system of endogenous anti-oxidant and anti-inflammatory adaptive responses as discussed by the authors.About:
This article is published in Pharmacological Research.The article was published on 2021-03-02. It has received 89 citations till now. The article focuses on the topics: Mechanism (biology).read more
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Hormesis: Wound Healing and Fibroblasts.
TL;DR: Hormetic dose responses are reported commonly in the dermal wound healing process, with the particular focus on cell viability, proliferation, migration and collagen deposition of human and murine fibroblasts with in vitro studies as discussed by the authors .
Journal ArticleDOI
The role of non-coding RNAs in ferroptosis regulation
TL;DR: An overview of the main mechanisms and targets of ferroptosis and non-coding RNA regulation can be found in this paper , where the authors focus on the mechanisms of RNA regulation.
Journal ArticleDOI
Hormesis and Oxidative Distress: Pathophysiology of Reactive Oxygen Species and the Open Question of Antioxidant Modulation and Supplementation
Mariapaola Nitti,Barbara Marengo,Anna Lisa Furfaro,Maria Adelaide Pronzato,Umberto M. Marinari,Cinzia Domenicotti,Nicola Traverso +6 more
TL;DR: The review herein provides an overview of the pathophysiological role of ROS and focuses the attention on positive and negative aspects of antioxidant modulation with the intent to find new insights for a successful clinical application.
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Hormesis and Endothelial Progenitor Cells
TL;DR: These studies demonstrate the capacity of these agents to enhance EPC proliferation and angiogenesis functional applications, having a focus on repairing endothelial tissue damage due to acute injury (e.g., stroke), as well as damage from chronic conditions and normal aging processes.
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Nutrition to Optimise Human Health—How to Obtain Physiological Substantiation?
TL;DR: In this paper, the authors demonstrate that a diet or a specific product optimizes health in the general population, which comes down to achieving perceived, non-medical or future health benefits in predominantly healthy persons.
References
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Nrf2-Keap1 defines a physiologically important stress response mechanism.
TL;DR: Analysis of keap1-knockout mice provides solid evidence that Keap1 acts as a negative regulator of Nrf2 and as a sensor of xenobiotic and oxidative stresses.
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Nrf2 signaling pathway: Pivotal roles in inflammation.
TL;DR: The members of the Keap1/Nrf2/ARE signal pathway and its downstream genes, the effects of this pathway on animal models of inflammatory diseases, and crosstalk with the NF-κB pathway are discussed.
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Expression of Nrf2 in Neurodegenerative Diseases
Chenere P. Ramsey,Charles A. Glass,Marshall B. Montgomery,Kathryn A. Lindl,Gillian P. Ritson,Luis A. Chia,Ronald L. Hamilton,Charleen T. Chu,Kelly L. Jordan-Sciutto +8 more
TL;DR: It is suggested that Nrf2-mediated transcription is not induced in neurons in AD despite the presence of oxidative stress, and in PD, nuclear localization of NRF2 is strongly induced, but this response may be insufficient to protect neurons from degeneration.
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When NRF2 Talks, Who's Listening?
TL;DR: This review highlights recent observations on the molecular interactions and their functional consequences between NRF2 and the arylhydrocarbon receptor (AhR), NF-κB, p53, and Notch1 signaling pathways, which provide a multi-tiered, integrated response to chemical stresses.
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Nrf2-mediated neuroprotection in the MPTP mouse model of Parkinson's disease : Critical role for the astrocyte
Pei Chun Chen,Marcelo R. Vargas,Amar K. Pani,Richard J. Smeyne,Delinda A. Johnson,Yuet Wai Kan,Jeffrey A. Johnson +6 more
TL;DR: Stark results indicate that Nrf2 expression restricted to astrocytes is sufficient to protect against MPTP andAstrocytic modulation of the NRF2-ARE pathway is a promising target for therapeutics aimed at reducing or preventing neuronal death in PD.