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The hormetic dose-response mechanism: Nrf2 activation

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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.
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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).

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Cerebrospinal fluid and plasma metabolomics of acute endurance exercise

TL;DR: In this paper , a broad-spectrum metabolomics was performed by liquid chromatography, tandem mass spectrometry (LCMS/MS) and correlation network analysis to identify a narrow but important channel of metabolic communication between the brain and body.
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Single cell RNA sequencing detects persistent cell type- and methylmercury exposure paradigm-specific effects in a human cortical neurodevelopmental model.

TL;DR: In this article, single-cell RNA sequencing (scRNAseq) was used to assess the persistent effects of methylmercury exposure in a differentiating cortical human-induced pluripotent stem cell (hiPSC) model which was exposed to in vivo relevant and non-cytotoxic MeHg (0.1 and 1.0μM) concentrations.
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Diet and exercise in lifestyle medicine: the hormetic effects of bioactive compounds on human health

TL;DR: In this paper , the role of bioactive compounds in the context of the hormetic-based lifestyle medicine is discussed, and the dose-response relationship of nutritional hormetins and exercise are non-linear and individual variability was found on the nuclear factor erythroid-2-related factor 2 (Nrf2) pathway in human studies.
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Long-term improvement by ozone treatment in chronic pain secondary to chemotherapy-induced peripheral neuropathy: A preliminary report

TL;DR: Most patients obtained clinically relevant and long-lasting improvement in chronic pain secondary to CIPN after treatment with ozone, and the toxicity grade, according to the Common Terminology Criteria for Adverse Events (CTCAE v.5), improved in half of the patients.
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Haematococcus Pluvialis Extends Yeast Lifespan and Improves Slc25a46 Gene Knockout-Associated Mice Phenotypic Defects.

TL;DR: In this article, the anti-aging effects of Haematococcus pluvialis extract were investigated in yeast and showed that it could effectively extend yeast chronological lifespan by reducing intracellular reactive oxygen species (ROS) levels, promoting mitochondrial membrane potential (MMP) levels and accumulating storage carbohydrate (glycogen).
References
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Journal ArticleDOI

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

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

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.
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