预约演示

更新于：2025-05-07

SEMA7A

更新于：2025-05-07

基本信息

别名

CD108、CDw108、H-Sema-L

+ [10]

简介

Plays an important role in integrin-mediated signaling and functions both in regulating cell migration and immune responses. Promotes formation of focal adhesion complexes, activation of the protein kinase PTK2/FAK1 and subsequent phosphorylation of MAPK1 and MAPK3. Promotes production of pro-inflammatory cytokines by monocytes and macrophages. Plays an important role in modulating inflammation and T-cell-mediated immune responses. Promotes axon growth in the embryonic olfactory bulb. Promotes attachment, spreading and dendrite outgrowth in melanocytes.

关联

项与 SEMA7A 相关的药物

WO2023235765

专利挖掘

靶点

SEMA7A

作用机制-

在研机构

Regents of the University of Colorado

原研机构

Regents of the University of Colorado

在研适应症

消化系统疾病 [+6]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

CN118598994

专利挖掘

靶点

SEMA7A

作用机制-

在研机构

苏州大学

原研机构

苏州大学

在研适应症

骨髓疾病 [+3]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

CN118598995

专利挖掘

靶点

SEMA7A

作用机制-

在研机构

苏州大学

原研机构

苏州大学

在研适应症

血液及淋巴系统疾病 [+2]

非在研适应症-

最高研发阶段药物发现

首次获批国家/地区-

首次获批日期1800-01-20

100 项与 SEMA7A 相关的临床结果

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100 项与 SEMA7A 相关的转化医学

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0 项与 SEMA7A 相关的专利（医药）

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299

项与 SEMA7A 相关的文献（医药）

2025-05-01·International Immunopharmacology

The characterization and validation of regulated cell death-related genes in chronic rhinosinusitis with nasal polyps

Article

作者: Qin, Gang ; Peng, Yi ; Yan, Pi-Jun ; Fei, Jing ; Teng, Fang-Yuan ; Xu, Yong ; Li, Hong-Xia ; Xu, Wei

BACKGROUNDRegulated cell death (RCD), a genetically controlled process mediated by specialized molecular pathways (commonly termed programmed cell death), plays pivotal roles in diverse pathophysiological processes. However, the landscape and functional implications of RCD subtypes in chronic rhinosinusitis with nasal polyps (CRSwNP) remain poorly characterized. This study aimed to systematically investigate the involvement of RCD mechanisms in the pathogenesis and progression of CRSwNP.METHODSTranscriptomic datasets (GSE136825, GSE23552, GSE198950, GSE196169, GSE156285) related to CRSwNP were retrieved from the Gene Expression Omnibus (GEO) database. A comprehensive panel of 18 RCD-associated gene sets was compiled through a systematic literature review. Gene set variation analysis (GSVA) was employed to profile RCD activation patterns in CRSwNP. Integrative bioinformatics approaches including weighted gene co-expression network analysis (WGCNA) and least absolute shrinkage and selection operator (LASSO) regression were implemented to identify hub RCD-related genes and construct a cell death index (CDI). Single-cell RNA sequencing (scRNA-seq) data were analyzed to map RCD dynamics across cellular subpopulations. Clinical validation was performed using qRT-PCR quantification of key genes in nasal polyp/inferior turbinate tissues, with the concurrent assessment of symptom severity via visual analogue scale (VAS) scores.RESULTSGSVA revealed significant upregulation of 8 RCD subtypes in CRSwNP: apoptosis, ferroptosis, necroptosis, entotic cell death, lysosome-dependent cell death, NETosis, immunogenic cell death, and anoikis. Pathway enrichment analysis demonstrated that RCD-related differentially expressed genes were predominantly involved in epithelial-mesenchymal transition (EMT) and immune-inflammatory regulation. Furthermore, the WGCNA algorithm and LASSO analysis identified 8 key cell death genes (PTHLH, GRINA, S100A9, SCG2, HMOX1, RNF183, TYROBP, SEMA7A), which were utilized to construct the cell death-related index (CDI). In training and validation cohorts, the CDI was significantly elevated in CRSwNP compared to control and exhibited high diagnostic performance, with elevated scores correlating with enhanced immune cell infiltration. Single-cell resolution analysis uncovered cell type-specific RCD activation patterns. Clinical validation confirmed significantly higher expression of S100A9, PTHLH, and HMOX1 in eosinophilic versus non-eosinophilic polyps. Notably, expression levels of PTHLH, S100A9, HMOX1, GRINA, and TYROBP showed strong positive correlations with VAS scores.CONCLUSIONSOur investigation delineates an RCD activation signature in CRSwNP pathogenesis, characterized by 8 key cell death modalities and their regulatory genes. The novel CDI exhibits promising diagnostic potential, while mechanistic insights suggest RCD pathways may drive disease progression through EMT potentiation and inflammatory cascade amplification. These findings provide a framework for developing RCD-targeted therapeutic strategies in CRSwNP.

2025-04-22·Stem Cells Translational Medicine

Reprogramming of skin fibroblasts by 3D spheroid culture promotes peripheral nerve regeneration via the ID3/semaphorin7a pathway

Article

作者: Xiong, Yinchun ; Shi, Chunmeng ; Qu, Langfan ; Zhang, Zhou ; Tan, Xu ; Chen, Zelin ; Li, Huijuan ; Cao, Xiaohui ; Wang, Yu

AbstractPeripheral nerve injury remains an intractable clinical issue with high morbidity, causing an excessive burden on the economy and society. Peripheral nerve tissue engineering combined with nerve conduits and supporting seed cells is considered a promising strategy for treating of long nerve defects. However, supporting seed cell sources that are easily accessible, capable of rapid expansion, and do not require genetic intervention are still urgently needed. This study intended to clarify whether the easily accessible and rapid expansion skin fibroblasts are the ideal supporting seed cells and can be reprogrammed into neural progenitor-like cells (NPCs) by forcing them to grow into a three-dimensional (3D) spheroid morphology. Results showed that 3D spheroid mouse dermal fibroblasts (MDFs) exhibited neural cell-like properties and could efficiently induce dorsal root ganglion neurons to extend the neurites. Transplantation of 3D spheroid MDFs significantly accelerated the regeneration of the sciatic nerve and improved the motor function of rats after transection compared to monolayer MDFs. Mechanism studies revealed that 3D spheroid culture significantly upregulated the expressions of the inhibitor of DNA binding 3 (ID3) and the hypoxia-inducible factor-1α (HIF-1α). The upregulation of the inhibitor of DNA binding 3 in 3D spheroid MDFs plays a critical role in acquiring NPC properties. Meanwhile, the upregulated ID3 and HIF-1α could synergistically upregulate semaphorin7a expression, which finally improved the extending of nerve axon in vitro and in vivo. This study may shed new light on treatments for peripheral nerve injury.

2025-03-01·Gene

Transcriptomic integration and ligand–receptor crosstalk reveal the underlying molecular mechanisms between hip cartilage and subchondral bone in osteonecrosis of femoral head

Article

作者: Lu, Xueliang ; Qian, Hang ; Wang, Pengbo ; Liu, Ruiyu ; Tian, Donghao ; Dang, Xiaoqian ; Zhu, Yingkang ; Wang, Xu

Osteonecrosis of femoral head (ONFH) is characterized not only by ischemic bone tissue necrosis but also by cartilage degeneration, which plays an essential role in the pathogenesis of ONFH. The molecular communication between tissues contributes to disease progression, however the communication between cartilage and subchondral bone in the progression of ONFH remains unclear. In this study, we integrated transcriptomic data from ONFH cartilage and subchondral bone, exploring common differentially expressed genes (DEGs), pathway and function enrichment analyses, the protein-protein interaction (PPI) network, and hub genes to comprehensively study molecular integration. Additionally, we explored the molecular crosstalk between and within cartilage and subchondral bone using ligand-receptor pairs and ONFH cartilage proteomic data. Finally, key genes and ligand-receptor pairs were validated by quantitative real-time PCR (qRT-PCR). There were 27 common DEGs and five hub genes in cartilage and subchondral bone. The defined hub genes included COL1A1, COLIA2, CTSK, SPARC, and MXRA5. Notably, pathways related to ossification, extracellular matrix, and collagen formation were significantly altered in ONFH. Ligand-receptor data combined with DEGs revealed 60 differentially expressed ligands and 51 differentially expressed receptors in cartilage and four ligands and three receptors in subchondral bone. In inter-tissue comparisons, ligands from chondrocytes predominantly paired with receptors on osteoblasts in the subchondral bone, such as FN1, MMP2, and FGF1. Conversely, ligands from osteoblasts and osteocytes in the subchondral bone frequently paired with chondrocyte receptors, including FN1, COL1A1, and SEMA7A. At the protein level, we identified thirteen ligands and one receptor, with COL3A1 being the most highly expressed ligand and CD82 the only differentially expressed receptor in ONFH. This study highlights common molecular mechanisms and ligand-receptor crosstalk between and within cartilage and subchondral bone in ONFH, offering new insights into the disease's pathophysiology and potential molecular targets for therapeutic intervention.

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