NLRP3: Role in ischemia/reperfusion injuries

Ghafouri‐Fard, Soudeh; Shoorei, Hamed; Poornajaf, Yadollah; Hussen, Bashdar Mahmud; Hajiesmaeili, Yasaman; Abak, Atefe; Taheri, Mohammad

doi:10.3389/fimmu.2022.926895

Cited by 13 publications

(9 citation statements)

References 94 publications

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“…In addition, TLR4 also rises brain ischemic lesions. The protein expression of TLR4, TNF- α , caspase-1, NLRP3, and IL-8 significantly increased in the cerebral ischemia-reperfusion mice model [ 103 ]. Oxidative stress markers such as nitric oxide and malondialdehyde are increased whereas superoxide dismutase is reduced in these mice brains.…”

Section: Inflammatory Signaling Pathway In Ad and Strokementioning

confidence: 99%

Common Signaling Pathways Involved in Alzheimer’s Disease and Stroke: Two Faces of the Same Coin

Das

Ganesh

Fatima-Shad

2023

ADR

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Alzheimer’s disease (AD) and stroke are two interrelated neurodegenerative disorders which are the leading cause of death and affect the neurons in the brain and central nervous system. Although amyloid-β aggregation, tau hyperphosphorylation, and inflammation are the hallmarks of AD, the exact cause and origin of AD are still undefined. Recent enormous fundamental discoveries suggest that the amyloid hypothesis of AD has not been proven and anti-amyloid therapies that remove amyloid deposition have not yet slowed cognitive decline. However, stroke, mainly ischemic stroke (IS), is caused by an interruption in the cerebral blood flow. Significant features of both disorders are the disruption of neuronal circuitry at different levels of cellular signaling, leading to the death of neurons and glial cells in the brain. Therefore, it is necessary to find out the common molecular mechanisms of these two diseases to understand their etiological connections. Here, we summarized the most common signaling cascades including autotoxicity, ApoE4, insulin signaling, inflammation, mTOR-autophagy, notch signaling, and microbiota-gut-brain axis, present in both AD and IS. These targeted signaling pathways reveal a better understanding of AD and IS and could provide a distinguished platform to develop improved therapeutics for these diseases.

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Section: Inflammatory Signaling Pathway In Ad and Strokementioning

confidence: 99%

Common Signaling Pathways Involved in Alzheimer’s Disease and Stroke: Two Faces of the Same Coin

Das

Ganesh

Fatima-Shad

2023

ADR

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“…The NOD-like receptor protein 3 (NLRP3) inflammasome is a protein complex located in the cells. Its main function is to activate the production of caspase-1, IL-1, and IL-18, thus promoting inflammation and apoptosis, and causing neuronal damage [ 167 ]. The NLRP3 inflammasome plays an important role in ischemia-induced inflammatory injury, and thioredoxin interacting protein (TXNIP) is closely related to the activation of NLRP3.…”

Section: The Role and Mechanism Of Nrf2 In Cerebral Ischemic Strokementioning

confidence: 99%

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

et al. 2022

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Cerebral ischemic stroke is characterized by acute ischemia in a certain part of the brain, which leads to brain cells necrosis, apoptosis, ferroptosis, pyroptosis, etc. At present, there are limited effective clinical treatments for cerebral ischemic stroke, and the recovery of cerebral blood circulation will lead to cerebral ischemia-reperfusion injury (CIRI). Cerebral ischemic stroke involves many pathological processes such as oxidative stress, inflammation, and mitochondrial dysfunction. Nuclear factor erythroid 2-related factor 2 (Nrf2), as one of the most critical antioxidant transcription factors in cells, can coordinate various cytoprotective factors to inhibit oxidative stress. Targeting Nrf2 is considered as a potential strategy to prevent and treat cerebral ischemia injury. During cerebral ischemia, Nrf2 participates in signaling pathways such as Keap1, PI3K/AKT, MAPK, NF-κB, and HO-1, and then alleviates cerebral ischemia injury or CIRI by inhibiting oxidative stress, anti-inflammation, maintaining mitochondrial homeostasis, protecting the blood–brain barrier, and inhibiting ferroptosis. In this review, we have discussed the structure of Nrf2, the mechanisms of Nrf2 in cerebral ischemic stroke, the related research on the treatment of cerebral ischemia through the Nrf2 signaling pathway in recent years, and expounded the important role and future potential of the Nrf2 pathway in cerebral ischemic stroke.

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Section: Introductionmentioning

confidence: 99%

“…Non-coding RNAs including long non-coding RNAs (lncRNAs) and miRNAs have been shown to influence I/R injury via regulating mitochondrial function, apoptotic and autophagic pathways, and signal transducers. 8,9 MicroRNA-146a (miR-146a) has been proved to be linked with the progression of several kinds of diseases. Conjugation of cerium oxide nanoparticles to miR-146a could improve diabetic wound healing by promoting angiogenesis and fibrotic processes, 10 but decreasing inflammation, oxidative stress.…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-146a Improved Acute Lung Injury Induced by hepatic Ischemia-reperfusion Injury by Inhibiting PRDX1

Chen

Yao

et al. 2023

Dose-Response

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Hepatic ischemia-reperfusion injury (HIRI)–induced acute lung injury (ALI) is characterized by high incidence and poor prognosis. The regulatory role of microRNA-146a (miR-146a) in HIRI has been reported, but if miR-146a could affect the progression of HIRI-induced ALI has not been reported. The mice HIRI model was established by ligating left hepatic portal vein and hepatic artery for 60 minutes and then treating with reperfusion for 4 hours. Hypoxia-reoxygenation (HR) was performed to establish cell model. The binding site between miR-146a and Peroxidase 1 (PRDX1) was predicted and validated. The levels of inflammation factors and redox markers were detected with commercial kits. Significant lower expression of miR-146a and higher expression of PRDX1 in HIRI animal model were observed. miR-146a inhibited the liver injury after HIRI induction through targeting PRDX1. miR-146a inhibited the lung injury caused by HIRI via regulating PRDX1. The inhibition of cell apoptosis and inflammation factors by miR-146a were reversed by pcDNA-PRDX1. This research demonstrated that miR-146a improved ALI caused by HIRI by inhibiting apoptosis, inflammation, oxidative condition through targeting PRDX1. This study might provide a novel thought for the prevention and treatment of ALI caused by HIRI by regulating miR-146a/PRDX1 axis.

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NLRP3: Role in ischemia/reperfusion injuries

Cited by 13 publications

References 94 publications

Common Signaling Pathways Involved in Alzheimer’s Disease and Stroke: Two Faces of the Same Coin

Common Signaling Pathways Involved in Alzheimer’s Disease and Stroke: Two Faces of the Same Coin

Nrf2 Regulates Oxidative Stress and Its Role in Cerebral Ischemic Stroke

MicroRNA-146a Improved Acute Lung Injury Induced by hepatic Ischemia-reperfusion Injury by Inhibiting PRDX1

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