RNF20 deletion causes inflammation in model of sepsis through the NLRP3 activation

Qi, Anlong; Liu, Yan-Cun; Zhai, Jianhua; Wang, Yongtao; Li, Wang; Wang, Tong; Chai, Yanfen

doi:10.1080/08923973.2023.2170241

Cited by 3 publications

(2 citation statements)

References 31 publications

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“…[6][7][8][9][10] Under inflammatory stimuli, the NLRP3 inflammasome becomes activated, triggering the release of proinflammatory cytokines such as interleukin-1β (IL-1β) and interleukin-18 (IL-18). [11][12][13][14][15] Emerging evidence highlights its pivotal role in the pathogenesis of diverse disorders, including rheumatoid arthritis, inflammatory bowel disease, and diabetes. [16,17] Nevertheless, its involvement in neuropathic pain and its interplay with early diagnosis and severity remain largely unexplored.…”

Section: Introductionmentioning

confidence: 99%

Correlation analysis between the early diagnosis and severity of neuropathic pain and the activation level of NLRP3 inflammasome: A retrospective study

Wang,

Zhou,

Zhou

2024

Medicine

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To investigate the correlation between neuropathic pain’s early diagnosis, severity, and nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing-3 (NLRP3) inflammasome activation, we retrospectively evaluated 50 patients with neuropathic pain and 50 healthy individuals. Activation of the NLRP3 inflammasome was measured in blood samples, as well as pain levels and clinical markers. Neuropathic pain patients exhibited elevated NLRP3 inflammasome activation. Pain intensity positively correlated with activation. Correlation was also observed with inflammatory markers and pain-related biomarkers. NLRP3 inflammasome demonstrated high diagnostic sensitivity. In conclusion, NLRP3 inflammasome activation influences neuropathic pain initiation and progression. Measuring activation levels may serve as an early diagnostic indicator and severity gauge for neuropathic pain.

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Section: Introductionmentioning

confidence: 99%

Correlation analysis between the early diagnosis and severity of neuropathic pain and the activation level of NLRP3 inflammasome: A retrospective study

Wang,

Zhou,

Zhou

2024

Medicine

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“…Studies have confirmed the essential role of RNF20 in several physiological processes including cell differentiation, spermatogenesis, and adipose tissue development (29,32,34). Furthermore, RNF20 deficiency in association with some pathological processes such oncogenesis and inflammation has also been extensively explored (35)(36)(37). Although the fundamental role of RNF20 has been recognized under both physiological and pathological conditions, the connection between RNF20 and its downstream target H2Bub1 in the ID context has never been systematically explored.…”

Section: Introductionmentioning

confidence: 99%

Iron deficiency–induced ferritinophagy impairs skeletal muscle regeneration through RNF20-mediated H2Bub1 modification

Che,

Li,

Wang

et al. 2023

Sci. Adv.

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Iron deficiency (ID) is a widespread condition concomitant with disease and results in systemic dysfunction of target tissues including skeletal muscle. Activated by ID, ferritinophagy is a recently found type of selective autophagy, which plays an important role in various physiological and pathological conditions. In this study, we demonstrated that ID-mediated ferritinophagy impeded myogenic differentiation. Mechanistically, ferritinophagy induced RNF20 degradation through the autophagy-lysosomal pathway and then negatively regulated histone H2B monoubiquitination at lysine-120 in the promoters of the myogenic markers MyoD and MyoG , which inhibited myogenic differentiation and regeneration. Conditional knockout of NCOA4 in satellite cells, overexpression of RNF20 or treatment with 3-methyladenine restored skeletal muscle regenerative potential under ID conditions. In patients with ID, RNF20 and H2Bub1 protein expression is downregulated in skeletal muscle. In conclusion, our study indicated that the ferritinophagy-RNF20-H2Bub1 axis is a pathological molecular mechanism underlying ID-induced skeletal muscle impairment, suggesting potential therapeutic prospects.

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The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis

Vastrad,

Vastrad

2024

Preprint

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Cardiac arrest (CA) is a common cause of death world wide. The disease has lacks effective treatment. Efforts have been made to elucidate the molecular pathogenesis of CA, but the molecular mechanisms remain elusive. To identify key genes and pathways in CA, the next generation sequencing (NGS) GSE200117 dataset was downloaded from the Gene Expression Omnibus (GEO) database. DESeq2 tool was used to recognize differentially expressed genes (DEGs). Gene ontology (GO) and REACTOME pathway enrichment analyses were performed to analyze the DEGs and associated signal pathways in the g:Profiler database. The IID database was used to construct the protein-protein interaction (PPI) network, and modules analysis was performed using Cytoscape. A miRNA-hub gene regulatory network and TF-hub gene regulatory network were then constructed to screen miRNAs, TFs and hub genes by miRNet and NetworkAnalyst database and Cityscape software. Receiver operating characteristic curve (ROC) analysis used to verified the hub genes. In total, 844 DEGs were identified, comprising 414 up regulated genes and 430 down regulated genes. GO and REACTOME pathway enrichment analyses indicated that the DEGs for CA were mainly enriched in organonitrogen compound metabolic process, response to stimulus, translation and immune system. Ten hub genes (up-regulated: HSPA8, HOXA1, INCA1 and TP53; down-regulated: HSPB1, LMNA, SNCA, ADAMTSL4 and PDLIM7) were screened. We also predicted miRNAs (hsa-mir-1914-5p and hsa-mir-598-3p) and TFs (JUN and PRRX2) targeting hub genes. This study uses a series of bioinformatics technologies to obtain hug genes, miRNAs and TFs, and key pathways related to CA. These analysis results provide us with new ideas for finding biomarkers and treatment methods for CA.

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RNF20 deletion causes inflammation in model of sepsis through the NLRP3 activation

Cited by 3 publications

References 31 publications

Correlation analysis between the early diagnosis and severity of neuropathic pain and the activation level of NLRP3 inflammasome: A retrospective study

Correlation analysis between the early diagnosis and severity of neuropathic pain and the activation level of NLRP3 inflammasome: A retrospective study

Iron deficiency–induced ferritinophagy impairs skeletal muscle regeneration through RNF20-mediated H2Bub1 modification

The Identification of Key Genes and Biological Pathways in Cardiac Arrest by Integrated Bioinformatics and Next Generation Sequencing Data Analysis

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