Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3

Huang, Wei; Hong, Yiyi; He, Weiqun; Jiang, Li; Deng, Wen; Peng, Biyan; Tang, Fen; Shen, Chaolan; Lan, Qianqian; Huang, Hui; Zhong, Haibin; Lv, Jian; Zeng, Siming; Li, Min; Ouyang, Yanling; Liang, Jie; Mo, Zhongxiang; Chen, Qi; Cui, Ling; Zhang, Mingyuan; Xu, Fan; Zhou, Zhou

doi:10.1007/s00011-022-01550-w

Cited by 7 publications

(2 citation statements)

References 63 publications

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“…Thus, SOCS3 downregulation could exacerbate inflammation. Additionally, SOCS3 can affect the differentiation of immune cells, particularly regulating the Th1/Th2 balance of T cells and the polarization of macrophages towards the M2 phenotype, thereby influencing the course of immune responses ( Huang W. et al, 2022 ). Recent studies have found an increase in SOCS3 expression in the hepatocytes of patients with NAFLD, which may be related to inflammation and insulin resistance in these conditions ( Zhang et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation

Zhong,

Xie,

Zhang

et al. 2024

Front. Pharmacol.

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Background: Non-alcoholic fatty liver disease (NAFLD) and atrial fibrillation (AF) are major health burdens, with emerging evidence suggesting NAFLD as a significant risk factor for AF, but the mechanism is remain unclear.Methods: In this study, we analyzed gene expression data from NAFLD (GSE89632) and AF (GSE75092) datasets from the Gene Expression Omnibus. We identified co-upregulated and co-downregulated genes between NAFLD and AF, assessed diagnostic potential of specific genes, conducted immune infiltration analysis, and performed molecular docking studies with sodium glucose co-transporter 2 inhibitors (SGLT2i).Results: We identified eight co-upregulated and 31 co-downregulated genes between NAFLD and AF. Genes such as AMOT, PDE11A, TYMS, TMEM98, and PTGS2 demonstrated substantial diagnostic potential for identifying NAFLD patients at risk of AF. Immune infiltration analysis discovered an elevated presence of CD8 T cells, γδ T cells, and M2 macrophages in NAFLD livers, linking systemic inflammation to NAFLD and AF. Additionally, studies have shown that a connection between mitochondrial dysfunction and several hub genes like DGAT1, TYMS, and PTGS2, suggesting that mitochondrial disturbances may underpin the systemic inflammation in NAFLD, which possibly exacerbating AF. Molecular docking studies indicated that empagliflozin's binding affinity with key genes such as DGAT1, TYMS, and PTGS2 presents a novel therapeutic avenue for NAFLD-associated AF.Conclusion: Our study firstly discovered that AMOT, PDE11A, TYMS, TMEM98, and PTGS2 are associated with NAFLD-related AF and hold strong diagnostic values. Our study also indicates that mitochondrial dysfunction and systemic inflammation may be potential mechanisms bridging NAFLD and AF. Additionally, we identified empagliflozin as a potentially effective therapeutic agent for NAFLD-related AF at the molecular structure level. These novel insights contribute to the further understanding, diagnosis, and intervention of NAFLD-related AF.

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Section: Discussionmentioning

confidence: 99%

Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation

Zhong,

Xie,

Zhang

et al. 2024

Front. Pharmacol.

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“…In recent years, there has been increased focus on the relationship between microglia M1/M2 polarization and neuroinflammation 41 . Notably, this inflammatory response can disrupt the BBB causing neurodegenerative diseases 42 .…”

Section: Discussionmentioning

confidence: 99%

Exploring the mechanism of luteolin by regulating microglia polarization based on network pharmacology and in vitro experiments

Wang,

Yin,

Jiang

et al. 2023

Sci Rep

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Neuroinflammation manifests following injury to the central nervous system (CNS) and M1/M2 polarization of microglia is closely associated with the development of this neuroinflammation. In this study, multiple databases were used to collect targets regarding luteolin and microglia polarization. After obtaining a common target, a protein–protein interaction (PPI) network was created and further analysis was performed to obtain the core network. Molecular docking of the core network with luteolin after gene enrichment analysis. In vitro experiments were used to examine the polarization of microglia and the expression of related target proteins. A total of 77 common targets were obtained, and the core network obtained by further analysis contained 38 proteins. GO and KEGG analyses revealed that luteolin affects microglia polarization in regulation of inflammatory response as well as the interleukin (IL)-17 and tumor necrosis factor (TNF) signaling pathways. Through in vitro experiments, we confirmed that the use of luteolin reduced the expression of inducible nitric oxide synthase (iNOS), IL-6, TNF-α, p-NFκBIA (p-IκB-α), p-NFκB p65, and MMP9, while upregulating the expression of Arg-1 and IL-10. This study reveals various potential mechanisms by which luteolin induces M2 polarization in microglia to inhibit the neuroinflammatory response.

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Mer activation ameliorates nerve injury-induced neuropathic pain by regulating microglial polarization and neuroinflammation via SOCS3 in male rats

Wang,

Zhu,

2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Cavin-1 promotes M2 macrophages/microglia polarization via SOCS3

Cited by 7 publications

References 63 publications

Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation

Identification of key genes increasing susceptibility to atrial fibrillation in nonalcoholic fatty liver disease and the potential mechanisms: mitochondrial dysfunction and systemic inflammation

Exploring the mechanism of luteolin by regulating microglia polarization based on network pharmacology and in vitro experiments

Mer activation ameliorates nerve injury-induced neuropathic pain by regulating microglial polarization and neuroinflammation via SOCS3 in male rats

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