NLRP3/miR-223-3p axis attenuates neuroinflammation induced by chronic intermittent hypoxia

Wu, Cheng; Xing, Wen; Zhang, Yuanxiang; Wang, Jue; Zuo, Na; Sun, Fuqin; Liu, Qi; Liu, Shaofeng

doi:10.1007/s10142-023-01268-w

Cited by 3 publications

(2 citation statements)

References 43 publications

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“…OSA alters exosomal carriers in circulation, especially miRNAs, and promotes endothelial dysfunction [68]. Several in vivo studies have demonstrated the involvement of miRNAs and the nucleotide-binding domain-like receptor protein 3 (NLRP3) inflammasome in chronic IH-induced inflammation and tissue injury [36, [69][70][71][72][73][74][75]. During IH exposures, miRNAs such as miR-155 [69], miR-210 [70], and miR-144 [71] are upregulated in renal tissue, endothelium, and serum-derived extracellular vesicles, respectively; the silencing of these miRNAs ameliorate IH-induced inflammation, endothelial dysfunction, and tissue injury [69][70][71].…”

Section: Mirna/nlrp3 Signalingmentioning

confidence: 99%

“…In animal models, chronic IH exposure increases NLRP3 inflammasome expression, and NLRP3 deficiency or inhibition protects against IH-induced inflammation, oxidative stress, and apoptosis in the brain, heart, and vasculature [36, [72][73][74][75]. Additionally, in vitro IH exposure fails to induce IL-1β overproduction in bone marrow-derived macrophages isolated from NLRP3 knockout male mice [87], reinforcing the involvement of NLRP3 in IH-induced inflammation.…”

Section: Mirna/nlrp3 Signalingmentioning

confidence: 99%

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Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring

Song,

Baker,

Watters

et al. 2024

IJMS

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Obstructive sleep apnea (OSA), a respiratory sleep disorder associated with cardiovascular diseases, is more prevalent in men. However, OSA occurrence in pregnant women rises to a level comparable to men during late gestation, creating persistent effects on both maternal and offspring health. The exact mechanisms behind OSA-induced cardiovascular diseases remain unclear, but inflammation and oxidative stress play a key role. Animal models using intermittent hypoxia (IH), a hallmark of OSA, reveal several pro-inflammatory signaling pathways at play in males, such as TLR4/MyD88/NF-κB/MAPK, miRNA/NLRP3, and COX signaling, along with shifts in immune cell populations and function. Limited evidence suggests similarities in pregnancies and offspring. In addition, suppressing these inflammatory molecules ameliorates IH-induced inflammation and tissue injury, providing new potential targets to treat OSA-associated cardiovascular diseases. This review will focus on the inflammatory mechanisms linking IH to cardiovascular dysfunction in males, pregnancies, and their offspring. The goal is to inspire further investigations into the understudied populations of pregnant females and their offspring, which ultimately uncover underlying mechanisms and therapeutic interventions for OSA-associated diseases.

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Section: Mirna/nlrp3 Signalingmentioning

confidence: 99%

Section: Mirna/nlrp3 Signalingmentioning

confidence: 99%

Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring

Song,

Baker,

Watters

et al. 2024

IJMS

View full text Add to dashboard Cite

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Exosomes from IH- Induced bEnd3 Cells Promote OSA Cognitive Impairment via miR-20a-5p/MFN2 Mediated Pyroptosis of HT22 Cells

Chen,

Shang,

et al. 2024

NSS

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Pyroptosis: An Accomplice in the Induction of Multisystem Complications Triggered by Obstructive Sleep Apnea

Han,

Ye,

Wang

2024

Biomolecules

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Obstructive sleep apnea (OSA) is a common respiratory disorder, primarily characterized by two pathological features: chronic intermittent hypoxia (CIH) and sleep deprivation (SD). OSA has been identified as a risk factor for numerous diseases, and the inflammatory response related to programmed cell necrosis is believed to play a significant role in the occurrence and progression of multisystem damage induced by OSA, with increasing attention being paid to pyroptosis. Recent studies have indicated that OSA can elevate oxidative stress levels in the body, activating the process of pyroptosis within different tissues, ultimately accelerating organ dysfunction. However, the molecular mechanisms of pyroptosis in the multisystem damage induced by OSA remain unclear. Therefore, this review focuses on four major systems that have received concentrated attention in existing research in order to explore the role of pyroptosis in promoting renal diseases, cardiovascular diseases, neurocognitive diseases, and skin diseases in OSA patients. Furthermore, we provide a comprehensive overview of methods for inhibiting pyroptosis at different molecular levels, with the goal of identifying viable targets and therapeutic strategies for addressing OSA-related complications.

show abstract

NLRP3/miR-223-3p axis attenuates neuroinflammation induced by chronic intermittent hypoxia

Cited by 3 publications

References 43 publications

Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring

Obstructive Sleep Apnea-Associated Intermittent Hypoxia-Induced Immune Responses in Males, Pregnancies, and Offspring

Exosomes from IH- Induced bEnd3 Cells Promote OSA Cognitive Impairment via miR-20a-5p/MFN2 Mediated Pyroptosis of HT22 Cells

Pyroptosis: An Accomplice in the Induction of Multisystem Complications Triggered by Obstructive Sleep Apnea

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