ZNF667 alleviates the inflammatory damage in intervertebral disc degeneration via inhibiting NF-κB signaling pathway.

{"sci_version": "1.2", "schema": "https://corpus.bntrg.co.uk/sci/1.0/sci.schema.json", "id": "pmid:40074310", "kind": "science-record", "revision": 2, "content_hash": "sha256:cedfd54dfe8e889a6b34eacf26534a01b64825ed3a6fe338b97d2c9840a5b947", "created_at": "2026-11-01T20:30:17Z", "updated_at": "2026-11-01T21:34:53Z", "generator": {"name": "corpus-assay-engine", "run_id": "reading-sci-2026-11-01"}, "paper": {"state": "complete", "title": "ZNF667 alleviates the inflammatory damage in intervertebral disc degeneration via inhibiting NF-κB signaling pathway.", "doi": "10.11817/j.issn.1672-7347.2024.240122", "pmid": "40074310", "authors": ["Hua Zhong", "Lebin Guo", "Yan Yang", "Chenjun Tian", "Fusheng Liu", "Bowen Zheng"], "journal": "Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences", "year": 2024, "abstract": "OBJECTIVES: With the aging population, the incidence of intervertebral disc degeneration (IDD) is increasing every year. The pathogenesis of IDD is complex, and there are currently no effective treatment options. This study aims to investigate the specific function and underlying mechanism of zinc finger protein 667 (ZNF667) in the inflammatory damage of nucleus pulposus cells in IDD.\nMETHODS: Differential expression genes (DEG) associated with IDD were screened from IDD-related datasets in the Gene Expression Omnibus (GEO) (GSE124272 and GSE150408), and ZNF667, which is closely related to gene transcriptional regulation, was selected and analyzed in several IDD-related datasets (GSE124272, GSE150408, GSE56081, GSE147383, GSE23130). Nucleus pulposus tissues were collected from 3 IDD patients and 3 trauma-induced vertebral fracture patients (serving as controls). Hematoxylin and eosin (HE) staining was performed for pathological examination, and immunohistochemistry (IHC) was used to assess ZNF667 expression in the nucleus pulposus tissues. Gene set enrichment analysis (GSEA) was then employed to elucidate the potential mechanisms of ZNF667. For in vitro validation, human primary nucleus pulposus cells were treated with 10 ng/mL of interleukin-1β (IL-1β) to establish an IDD cell model, and subsequently transfected with a ZNF667 overexpression plasmid. Flow cytometry was used to evaluate cell apoptosis, enzyme-linked immunosorbent assay (ELISA) measured the levels of inflammatory factors-cyclooxygenase-2 (COX-2), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) in the cell culture supernatant, real-time polymerase chain reaction (RT-PCR) quantified ZNF667 mRNA expression, and Western blotting assessed protein expression levels of ZNF667, myeloid differentiation factor 88 (MyD88), P65, and phosphorylated P65 (p-P65).\nRESULTS: Analysis of both the GEO datasets and clinical tissue samples revealed that ZNF667 expression is reduced in IDD. In IDD patients, the extracellular matrix and nucleus pulposus cells are significantly diminished, and the arrangement of fibrochondrocytes is disordered. GSEA results showed that ZNF667 may be involved in biological processes such as angiogenesis, epithelial-mesenchymal transition (EMT), oxidative phosphorylation, peroxisome function, steroid biosynthesis, and the NF-κB-mediated TNF-α signaling pathway. In vitro, ZNF667 was expressed at low levels in the IL-1β-induced IDD cell model, and overexpression of ZNF667 reversed the IL-1β-induced increase in cell apoptosis, the upregulation of inflammation factors (COX-2, IL-6, TNF-α), and the increased expression of NF-κB pathway-related proteins (MyD88 and the p-P65/P65 ratio) (all P<0.05).\nCONCLUSIONS: ZNF667 can alleviate nucleus pulposus cell apoptosis and inflammatory responses by inhibiting the NF-κB signaling pathway, thereby exerting a protective effect on intervertebral discs. This finding not only provides new insights into the pathogenesis of IDD but also suggests a potential therapeutic target for its treatment.", "claims": [{"id": "claim-method", "statement": "使用GraphPad Prism 7软件进行数据分析，数据以均数±标准差表示，采用t检验进行2组间的比较，P<0.05为差异有统计学意义。", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:40074310", "locator": "sections[17] \"统计学处理\" paragraph 2", "quote": "使用GraphPad Prism 7软件进行数据分析，数据以均数±标准差表示，采用t检验进行2组间的比较，P<0.05为差异有统计学意义。"}], "state": "complete"}, {"id": "claim-data-access", "statement": "选取基因表达综合 (gene expression omnibus，GEO)数据库中2个IDD相关基因数据集GSE124272(包括8例IDD患者和8例健康对照者的样本)、GSE150408(包括17例未经过治疗的IDD患者和17例健康对照者的样本)，利用R语言包及limma工具包对2个数据集进行分析，经过交叉筛选得到差异表达基因(differential expression gene，DEG)[log2|差异倍数(fold change，FC)|>0.60，P<0.05]。", "kind": "methodological", "target": null, "evidence": [{"asset": "source:pmid:40074310", "locator": "sections[7] \"筛选差异表达基因\" paragraph 2", "quote": "选取基因表达综合 (gene expression omnibus，GEO)数据库中2个IDD相关基因数据集GSE124272(包括8例IDD患者和8例健康对照者的样本)、GSE150408(包括17例未经过治疗的IDD患者和17例健康对照者的样本)，利用R语言包及limma工具包对2个数据集进行分析，经过交叉筛选得到差异表达基因(differential expression gene，DEG)[log2|差异倍数(fold change，FC)|>0.60，P<0.05]。"}], "state": "complete"}, {"id": "claim-target-result", "statement": "ZNF667可通过抑制NF-κB信号通路，减轻髓核细胞凋亡和炎症反应，发挥对椎间盘的保护作用。", "kind": "qualitative", "target": null, "evidence": [{"asset": "source:pmid:40074310", "locator": "sections[0] \"Abstract\" paragraph 4", "quote": "ZNF667可通过抑制NF-κB信号通路，减轻髓核细胞凋亡和炎症反应，发挥对椎间盘的保护作用。"}], "state": "complete"}], "gaps": []}, "experiment": {"state": "complete", "objective": "ZNF667可通过抑制NF-κB信号通路，减轻髓核细胞凋亡和炎症反应，发挥对椎间盘的保护作用。", "steps": [{"id": "read_published_estimate", "order": 1, "name": "Read the published estimate from the source", "kind": "other", "state": "complete", "blocked_on": null, "description": "The claim, method and evidence span published with the source article.", "duration_hours": null, "parameters": {}, "inputs": ["source:pmid:40074310"], "outputs": ["the published estimate and its evidence"], "instruments": [], "reagents": []}, {"id": "obtain_source_data", "order": 2, "name": "Obtain the source data from the named repository", "kind": "data-preparation", "state": "complete", "blocked_on": null, "description": "The GEO series accession resolves and its sample accessions are listed. 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null, "access": "open", "state": "resolved", "reader": null, "reader_status": "reader_required", "identifier": "GSE150408", "version": null, "note": "选取基因表达综合 (gene expression omnibus，GEO)数据库中2个IDD相关基因数据集GSE124272(包括8例IDD患者和8例健康对照者的样本)、GSE150408(包括17例未经过治疗的IDD患者和17例健康对照者的样本)，利用R语言包及limma工具包对2个数据集进行分析，经过交叉筛选得到差异表达基因(differential expression gene，DEG)[log2|差异倍数(fold change，FC)|>0.60，P<0.05]。", "structure": {"repository": "GEO", "access_route": "GEO accession URL", "access_statement_verbatim": "选取基因表达综合 (gene expression omnibus，GEO)数据库中2个IDD相关基因数据集GSE124272(包括8例IDD患者和8例健康对照者的样本)、GSE150408(包括17例未经过治疗的IDD患者和17例健康对照者的样本)，利用R语言包及limma工具包对2个数据集进行分析，经过交叉筛选得到差异表达基因(differential expression gene，DEG)[log2|差异倍数(fold change，FC)|>0.60，P<0.05]。", "access_statement_kind": "repository_route_statement", "sample_accessions": ["GSM4548691", "GSM4548692", "GSM4548693", "GSM4548694", "GSM4548695", "GSM4548696", "GSM4548697", "GSM4548698", "GSM4548699", "GSM4548700", "GSM4548701", "GSM4548702", "GSM4548703", 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