Recent Advances in Understanding Nrf2 Agonism and Its Potential Clinical Application to Metabolic and Inflammatory Diseases

Kim, Min-Ji; Jeon, Jae‐Han

doi:10.3390/ijms23052846

Cited by 35 publications

(34 citation statements)

References 269 publications

(326 reference statements)

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“…Protecting neuron from oxidative damage is potential hopeful strategy for treating MUD. Nrf2 is a key transcriptional regulator that keeps REDOX homeostasis by activating the anti-inflammatory, antioxidant, and cell-protective gene expression [ 6 ]. Nrf2 can affect the function of neurons strongly by decreasing the level of reactive oxygen species, which is conducive to survival and neurogenesis [ 67 ].…”

Section: The Important Role Of Nrf2 In Meth-induced Oxidative Stressmentioning

confidence: 99%

“…It is essential to explore the intrinsic damage mechanism of MUD, at meanwhile, to note the key initiating role of oxidative stress in MUD. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a crucial endogenous antioxidant factor [ 6 ]. It shows potential natural or pharmacological protective functions in a variety of diseases, including MUD [ 7 ].…”

Section: Introductionmentioning

confidence: 99%

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Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress

Chen

Xiong

et al. 2022

Oxidative Medicine and Cellular Longevity

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Methamphetamine can cause oxidative stress-centered lipid peroxidation, endoplasmic reticulum stress, mitochondrial dysfunction, excitatory neurotoxicity, and neuroinflammation and ultimately lead to nerve cell apoptosis, abnormal glial cell activation, and dysfunction of blood-brain barrier. Protecting nerve cells from oxidative destroy is a hopeful strategy for treating METH use disorder. Nrf2 is a major transcriptional regulator that activates the antioxidant, anti-inflammatory, and cell-protective gene expression through endogenous pathways that maintains cell REDOX homeostasis and is conducive to the survival of neurons. The Nrf2-mediated endogenous antioxidant pathway can also prevent neurodegenerative effects and functional defects caused by METH oxidative stress. Moderate exercise activates this endogenous antioxidant system, which involves in many diseases, including neurodegenerative diseases. Based on evidence from existing literature, we argue that appropriate exercise can play an endogenous antioxidant regulatory role in the Nrf2 signaling pathway to reduce a number of issues caused by METH-induced oxidative stress. However, more experimental evidence is needed to support this idea. In addition, further exploration is necessary about the different effects of various parameters of exercise intervention (such as exercise mode, time, and intensity) on the Nrf2 signaling pathway intervention. Whether there are synergistic effects between exercise and plant-derived Nrf2 activators is worth further investigation.

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Section: The Important Role Of Nrf2 In Meth-induced Oxidative Stressmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress

Chen

Xiong

et al. 2022

Oxidative Medicine and Cellular Longevity

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“…Abnormal levels of reactive oxygen species and a decreased capacity of mitochondria to produce DNA and therefore adjust to different metabolic conditions can be further worsened by certain drugs, like chemotherapeutic agents or Nrf2-inhibitors, and lack of anti-oxidants introduced via diet and supplements [ 25 , 26 ] ( Table 1 ).…”

Section: Possible Gene-environment Interactions In Phelan–mcdermid Sy...mentioning

confidence: 99%

Phenotypic Variability in Phelan–McDermid Syndrome and Its Putative Link to Environmental Factors

Boccuto

Mitz

Abenavoli

et al. 2022

Genes

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Phelan–McDermid syndrome (PMS) is a multi-systemic disorder characterized by both genetic and phenotypic variability. Genetic abnormalities causing PMS span from pathogenic variants of the SHANK3 gene to chromosomal rearrangements affecting the 22q13 region and leading to the loss of up to over nine megabases. The clinical presentation of individuals with PMS includes intellectual disability, neonatal hypotonia, delayed or absent speech, developmental delay, and minor dysmorphic facial features. Several other features may present with differences in age of onset and/or severity: seizures, autism, regression, sleep disorders, gastrointestinal problems, renal disorders, dysplastic toenails, and disrupted thermoregulation. Among the causes of this phenotypic variability, the size of the 22q13 deletion has effects that may be influenced by environmental factors interacting with haploinsufficiency or hemizygous variants of certain genes. Another mechanism linking environmental factors and phenotypic variability in PMS involves the loss of one copy of genes like BRD1 or CYP2D6, located at 22q13 and involved in the regulation of genomic methylation or pharmacokinetics, which are also influenced by external agents, such as diet and drugs. Overall, several non-mutually exclusive genetic and epigenetic mechanisms interact with environmental factors and may contribute to the clinical variability observed in individuals with PMS. Characterization of such factors will help to better manage this disorder.

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“…Nrf2 also plays a critical role in cardiovascular disease [6], and Nrf2 targeted activation might open new avenues in cardiovascular disease therapeutics. In addition to carcinogenesis and cardiovascular disease, studies have shown the role Nrf2 in diabetes complications and neurological disorders [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

The Therapeutic Potential of Kaemferol and Other Naturally Occurring Polyphenols Might Be Modulated by Nrf2-ARE Signaling Pathway: Current Status and Future Direction

Hussain

Khan²,

Alsharif³

et al. 2022

Molecules

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Kaempferol is a natural flavonoid, which has been widely investigated in the treatment of cancer, cardiovascular diseases, metabolic complications, and neurological disorders. Nrf2 (nuclear factor erythroid 2-related factor 2) is a transcription factor involved in mediating carcinogenesis and other ailments, playing an important role in regulating oxidative stress. The activation of Nrf2 results in the expression of proteins and cytoprotective enzymes, which provide cellular protection against reactive oxygen species. Phytochemicals, either alone or in combination, have been used to modulate Nrf2 in cancer and other ailments. Among them, kaempferol has been recently explored for its anti-cancer and other anti-disease therapeutic efficacy, targeting Nrf2 modulation. In combating cancer, diabetic complications, metabolic disorders, and neurological disorders, kaempferol has been shown to regulate Nrf2 and reduce redox homeostasis. In this context, this review article highlights the current status of the therapeutic potential of kaempferol by targeting Nrf2 modulation in cancer, diabetic complications, neurological disorders, and cardiovascular disorders. In addition, we provide future perspectives on kaempferol targeting Nrf2 modulation as a potential therapeutic approach.

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Recent Advances in Understanding Nrf2 Agonism and Its Potential Clinical Application to Metabolic and Inflammatory Diseases

Cited by 35 publications

References 269 publications

Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress

Potential Effects of Nrf2 in Exercise Intervention of Neurotoxicity Caused by Methamphetamine Oxidative Stress

Phenotypic Variability in Phelan–McDermid Syndrome and Its Putative Link to Environmental Factors

The Therapeutic Potential of Kaemferol and Other Naturally Occurring Polyphenols Might Be Modulated by Nrf2-ARE Signaling Pathway: Current Status and Future Direction

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