The Role of Nonneuronal Nrf2 Pathway in Ischemic Stroke: Damage Control and Potential Tissue Repair

Yang, Tuo; Sun, Yang; Zhang, Feng

doi:10.1007/978-3-319-32337-4_18

Cited by 3 publications

(2 citation statements)

References 135 publications

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“…Aside from excitotoxicity-induced neuronal cell death, oxidative stress may also elicit cell loss in CNS injury conditions. The predominant ROS are the superoxide anion (O 2 ▪ ), hydrogen peroxide (H 2 O 2 ), hydroxyl radical ( ▪ OH), peroxyl (RO 2 ▪ ), peroxynitrite anion (ONOO ▪ ), and nitrogen dioxide ( ▪ NO2) (Dhawan, 2014; Yang et al ., 2016). Excessive intracellular Ca 2+ accumulation results in overactivation of calcium-dependent enzymes such as nicotinamide adenine dinucleotide phosphate oxidase (NOX) and xanthine oxidase, both of which are capable of producing ROS.…”

Section: Pparγ Protects Against Cns Injurymentioning

confidence: 99%

Peroxisome proliferator-activated receptor γ (PPARγ): A master gatekeeper in CNS injury and repair

Cai

Yang

Liu

et al. 2018

Progress in Neurobiology

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184

147

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Peroxisome proliferator-activated receptor γ (PPARγ) is a widely expressed ligand-modulated transcription factor that governs the expression of genes involved in inflammation, redox equilibrium, trophic factor production, insulin sensitivity, and the metabolism of lipids and glucose. Synthetic PPARγ agonists (e.g. thiazolidinediones) are used to treat Type II diabetes and have the potential to limit the risk of developing brain injuries such as stroke by mitigating the influence of comorbidities. If brain injury develops, PPARγ serves as a master gatekeeper of cytoprotective stress responses, improving the chances of cellular survival and recovery of homeostatic equilibrium. In the acute injury phase, PPARγ directly restricts tissue damage by inhibiting the NFκB pathway to mitigate inflammation and stimulating the Nrf2/ARE axis to neutralize oxidative stress. During the chronic phase of acute brain injuries, PPARγ activation in injured cells culminates in the repair of gray and white matter, preservation of the blood-brain barrier, reconstruction of the neurovascular unit, resolution of inflammation, and long-term functional recovery. Thus, PPARγ lies at the apex of cell fate decisions and exerts profound effects on the chronic progression of acute injury conditions. Here, we review the therapeutic potential of PPARγ in stroke and brain trauma and highlight the novel role of PPARγ in long-term tissue repair. We describe its structure and function and identify the genes that it targets. PPARγ regulation of inflammation, metabolism, cell fate (proliferation/differentiation/maturation/survival), and many other processes also has relevance to other neurological diseases. Therefore, PPARγ is an attractive target for therapies against a number of progressive neurological disorders.

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Section: Pparγ Protects Against Cns Injurymentioning

confidence: 99%

Peroxisome proliferator-activated receptor γ (PPARγ): A master gatekeeper in CNS injury and repair

Cai

Yang

Liu

et al. 2018

Progress in Neurobiology

Self Cite

184

147

View full text Add to dashboard Cite

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“…In stroke, Nrf2 pathway is activated in both in vitro and in vivo ischemic models. In addition, to mediate self-defense in neurons, Nrf2 also actively regulates the expression of cytoprotective enzymes in other cell types within the neurovascular unit (NVU), including astrocytes and endothelial cells (ECs), and thus supports neuronal function and survival through cell–cell interaction (Yang et al, 2016). …”

Section: Support Of Energy Metabolism and Antioxidant Effects Of Astrmentioning

confidence: 99%

The Role of Astrocytes in Neuroprotection after Brain Stroke: Potential in Cell Therapy

Becerra-Calixto

Cardona‐Gómez

2017

Front. Mol. Neurosci.

196

151

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Astrocytes are commonly involved in negative responses through their hyperreactivity and glial scar formation in excitotoxic and/or mechanical injuries. But, astrocytes are also specialized glial cells of the nervous system that perform multiple homeostatic functions for the survival and maintenance of the neurovascular unit. Astrocytes have neuroprotective, angiogenic, immunomodulatory, neurogenic, and antioxidant properties and modulate synaptic function. This makes them excellent candidates as a source of neuroprotection and neurorestoration in tissues affected by ischemia/reperfusion, when some of their deregulated genes can be controlled. Therefore, this review analyzes pro-survival responses of astrocytes that would allow their use in cell therapy strategies.

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Mobilizing endogenous neuroprotection: the mechanism of the protective effect of acupuncture on the brain after stroke

Fu,

Wang,

et al. 2024

Front. Neurosci.

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Given its high morbidity, disability, and mortality rates, ischemic stroke (IS) is a severe disease posing a substantial public health threat. Although early thrombolytic therapy is effective in IS treatment, the limited time frame for its administration presents a formidable challenge. Upon occurrence, IS triggers an ischemic cascade response, inducing the brain to generate endogenous protective mechanisms against excitotoxicity and inflammation, among other pathological processes. Stroke patients often experience limited recovery stages. As a result, activating their innate self-protective capacity [endogenous brain protection (EBP)] is essential for neurological function recovery. Acupuncture has exhibited clinical efficacy in cerebral ischemic stroke (CIS) treatment by promoting the human body's self-preservation and “Zheng Qi” (a term in traditional Chinese medicine (TCM) describing positive capabilities such as self-immunity, self-recovery, and disease prevention). According to research, acupuncture can modulate astrocyte activity, decrease oxidative stress (OS), and protect neurons by inhibiting excitotoxicity, inflammation, and apoptosis via activating endogenous protective mechanisms within the brain. Furthermore, acupuncture was found to modulate microglia transformation, thereby reducing inflammation and autoimmune responses, as well as promoting blood flow restoration by regulating the vasculature or the blood–brain barrier (BBB). However, the precise mechanism underlying these processes remains unclear. Consequently, this review aims to shed light on the potential acupuncture-induced endogenous neuroprotective mechanisms by critically examining experimental evidence on the preventive and therapeutic effects exerted by acupuncture on CIS. This review offers a theoretical foundation for acupuncture-based stroke treatment.

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The Role of Nonneuronal Nrf2 Pathway in Ischemic Stroke: Damage Control and Potential Tissue Repair

Cited by 3 publications

References 135 publications

Peroxisome proliferator-activated receptor γ (PPARγ): A master gatekeeper in CNS injury and repair

Peroxisome proliferator-activated receptor γ (PPARγ): A master gatekeeper in CNS injury and repair

The Role of Astrocytes in Neuroprotection after Brain Stroke: Potential in Cell Therapy

Mobilizing endogenous neuroprotection: the mechanism of the protective effect of acupuncture on the brain after stroke

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