Suppression of cGAS/STING pathway-triggered necroptosis in the hippocampus relates H2S to attenuate cognitive dysfunction of Parkinson's disease DOI
Xinli Huang, Yu Hu, Jiang Wu

et al.

Experimental Neurology, Journal Year: 2024, Volume and Issue: 385, P. 115093 - 115093

Published: Dec. 19, 2024

Language: Английский

Mitochondrial DNA leakage: underlying mechanisms and therapeutic implications in neurological disorders DOI Creative Commons
Guangming Zhang,

Huayuan Wei,

Anliu Zhao

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Feb. 7, 2025

Mitochondrial dysfunction is a pivotal instigator of neuroinflammation, with mitochondrial DNA (mtDNA) leakage as critical intermediary. This review delineates the intricate pathways leading to mtDNA release, which include membrane permeabilization, vesicular trafficking, disruption homeostatic regulation, and abnormalities in dynamics. The escaped activates cytosolic sensors, especially cyclic gmp-amp synthase (cGAS) signalling inflammasome, initiating neuroinflammatory cascades via pathways, exacerbating spectrum neurological pathologies. therapeutic promise targeting discussed detail, underscoring necessity for multifaceted strategy that encompasses preservation homeostasis, prevention leakage, reestablishment dynamics, inhibition activation sensors. Advancing our understanding complex interplay between neuroinflammation imperative developing precision interventions disorders.

Language: Английский

Citations

3
The neuroimmune nexus: unraveling the role of the mtDNA-cGAS-STING signal pathway in Alzheimer’s disease DOI Creative Commons

Shuiyue Quan,

Xiaofeng Fu,

Huimin Cai

et al.

Molecular Neurodegeneration, Journal Year: 2025, Volume and Issue: 20(1)

Published: March 4, 2025

The relationship between Alzheimer's disease (AD) and neuroimmunity has gradually begun to be unveiled. Emerging evidence indicates that cyclic GMP-AMP synthase (cGAS) acts as a cytosolic DNA sensor, recognizing damage-associated molecular patterns (DAMPs), inducing the innate immune response by activating stimulator of interferon genes (STING). Dysregulation this pathway culminates in AD-related neuroinflammation neurodegeneration. A substantial body mitochondria are involved critical pathogenic mechanisms AD, whose damage leads release mitochondrial (mtDNA) into extramitochondrial space. This leaked mtDNA serves DAMP, various pattern recognition receptors defense networks brain, including cGAS-STING pathway, ultimately leading an imbalance homeostasis. Therefore, modulation mtDNA-cGAS-STING restore neuroimmune homeostasis may offer promising prospects for improving AD treatment outcomes. In review, we focus on during stress activation pathway. Additionally, delve research progress further discuss primary directions potential hurdles developing targeted therapeutic drugs, gain deeper understanding pathogenesis provide new approaches its therapy.

Language: Английский

Citations

1
Bibliometric Analysis of Neuroinflammation and Postoperative Cognitive Dysfunction DOI Creative Commons
Zheping Chen,

Zhenxiang Zuo,

Yizheng Zhang

et al.

Brain and Behavior, Journal Year: 2025, Volume and Issue: 15(1)

Published: Jan. 1, 2025

ABSTRACT Background The occurrence and development of postoperative cognitive dysfunction (POCD) are closely linked to neuroinflammation. This bibliometric analysis aims provide novel insights into the research trajectory, key topics, potential future trends in field neuroinflammation‐induced POCD. Methods Web Science Core Collection (WoSCC) database was searched identify publications from 2012 2023 on Bibliometric analysis, involving both statistical visual analyses, conducted using CiteSpace, VOSviewer, R software. Results Research POCD has exhibited an increasing trend over past 12 years. China had highest number publications, Nanjing Medical University most collaboration with other institutions, Zhiyi Zuo published author, Journal Neuroinflammation served as primary publication frequent keyword Keyword clustering indicated that predominant cluster is dexmedetomidine. Burst detection revealed delirium (POD), perioperative neurocognitive disorders (PND), apoptosis, epigenetic modifications were trends. Conclusions Our identified following areas associated POCD: anesthesia, surgery, dexmedetomidine, NLRP3 inflammasome, mechanism topics comprise POD, PND, modifications.

Language: Английский

Citations

0
PCSK9 exacerbates sevoflurane-induced neuroinflammatory response and apoptosis by up-regulating cGAS-STING signal DOI Creative Commons
Tao Su, Y. Si

Tissue and Cell, Journal Year: 2025, Volume and Issue: 93, P. 102739 - 102739

Published: Jan. 14, 2025

Language: Английский

Citations

0
Therapeutic potential of targeting the IRF2/POSTN/Notch1 axis in nucleus pulposus cells for intervertebral disc degeneration DOI Creative Commons
Daxue Zhu,

Zhaoheng Wang,

Shi‐Jie Chen

et al.

Journal of Neuroinflammation, Journal Year: 2025, Volume and Issue: 22(1)

Published: Jan. 22, 2025

Intervertebral disc degeneration (IDD) is a leading cause of low back pain, often linked to inflammation and pyroptosis in nucleus pulposus (NP) cells. The role Periostin (POSTN) IDD remains unclear. This study aims investigate the influence POSTN on NLRP3 inflammasome activation NP cells during IDD. IVD samples were collected from patients undergoing spinal surgery classified according Pfirrmann grading system. Human cultured treated with IL-1β induce pyroptotic phenotype. Western blotting, Immunofluorescence (IF), immunohistochemistry (IHC) assessed expression levels relevant proteins. Chromatin immunoprecipitation (ChIP) luciferase reporter assays verified binding IRF2 GSDMD promoters evaluated target genes. severity was using MRI histological analysis. Deletion significantly alleviated by suppressing activity found aggravate cell activating through NF-κB (P65) cGAS/STING signaling pathways. Furthermore, interacted Notch1 expression. identified as regulator at transcriptional level, contributing pyroptosis. also directly induced GSDMD, mediating Chemical screening Glucosyringic acid (GA) direct inhibitor POSTN, which delayed progression. elucidates pivotal highlights GA promising therapeutic candidate for These findings provide new insights into molecular mechanisms potential avenues treatment.

Language: Английский

Citations

0
Nrf2 Ameliorates Sevoflurane-Induced Cognitive Deficits in Aged Mice by Inhibiting Neuroinflammation in the Hippocampus DOI
Junhua Li, Jinfeng Li, Yafang Liu

et al.

Molecular Neurobiology, Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 19, 2025

Language: Английский

Citations

0
Histone lactylation protects against sevoflurane-induced cognitive impairment by regulating YTHDF3/PRDX3 mediated microglial pyroptosis in neonatal mice DOI
Yang Zhang,

Xiaowen Meng,

Weiming Zhao

et al.

International Immunopharmacology, Journal Year: 2025, Volume and Issue: 151, P. 114269 - 114269

Published: Feb. 28, 2025

Language: Английский

Citations

0
Mitigation of the toxic effects of nitrite: role and mechanism of isoleucine in mitigating mitochondrial DNA leakage-induced inflammation in grass carp (Ctenopharyngodon idella) under nitrite exposure DOI
Kaixuan Ren, Lin Feng, Pei Wu

et al.

Journal of Hazardous Materials, Journal Year: 2025, Volume and Issue: unknown, P. 138016 - 138016

Published: March 1, 2025

Language: Английский

Citations

0
Leucine enhances the cGAS-STING-NLRP3 pathway in autoimmune thyroiditis DOI Creative Commons
Xin Shen, Tingting Feng, Shangbin Li

et al.

Journal of Translational Autoimmunity, Journal Year: 2025, Volume and Issue: unknown, P. 100284 - 100284

Published: March 1, 2025

Language: Английский

Citations

0
High-cellulose diet ameliorates cognitive impairment by modulating gut microbiota and metabolic pathways in mice DOI
Moeka Tanabe, Kazuo Kunisawa, Isao Saito

et al.

Journal of Nutrition, Journal Year: 2025, Volume and Issue: unknown

Published: April 1, 2025

Language: Английский

Citations

0