详细内容（前10条）

1. ⭐ GSE311609 人类肺癌和乳腺癌FFPE样本的单细胞空间转录组学研究

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、single-cell、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Krisztian Homicsko ; Raphael GottardoSeries Type : OtherOrganism : Homo sapiensWe profiled human lung and breast tumor fragments using imaging-based single-cell spatial transcriptomics (10x Xenium) and compared the results to sequencing-based spatial transcriptomics (10x Visium) and single-nucleus RNA-seq
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2. ⭐ GSE294277 整合单细胞RNA测序和空间转录组学揭示了股骨髋臼撞击综合征和骨关节炎患者髋关节滑膜中巨噬细胞-成纤维细胞相互作用的差异

• ✍️ 作者：未知作者
• 🏷️ 关键词：macrophage、sequencing、spatial、spatial transcriptomics、transcriptomics
• 📝 描述：Contributors : Chia-Lung Wu ; Gulzada KulzhanovaSeries Type : Expression profiling by high throughput sequencing ; OtherOrganism : Homo sapiensFemoroacetabular impingement (FAI) and synovitis have been recognized as essential factors for developing osteoarthritis (OA) in the hip joints. However, little is known about altered synovial cellular compositions, their associated transcriptomic profiles, and cell-cell interactions between patients with FAI and hip OA. In the current study, by using integrative single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (Spatial-seq), we identified the molecular mechanisms by which synovial cells promote hip OA pathogenesis from FAI. Compared to FAI synovium, epiregulin (EREG)-enriched lining fibroblast-like synoviocytes (FLS) were significantly increased in the hip OA synovium. These EREG+ FLS are pro-inflammatory due to their high expression of CXCL1, IL8 (CXCL8), and MMPs. Furthermore, pseudotime analysis predicts that EREG+ FLS are potentially derived from DPP4+PI16+ sublining FLS. Importantly, analysis of cell-cell interactions indicates that fibroblast growth factor 2 (FGF2) secreted from COL1A1+IGFBP5+ fibrotic macrophages may signal through syndecan 4 (SDC4) expressed by EREG+ lining FLS, inducing the expression of IL6, IL8, MMP1, and PTGS2. The GO term analysis of activated genes downstream of FGF2-SDC4 signaling revealed that biological processes associated with inflammation and angiogenesis were upregulated in hip OA, while mechanical stimulus and skeletal muscle differentiation were dominant in FAI. Moreover, we also found that EREG+CCL20+MMP3hi lining FLS as well as most macrophage and monocyte populations are unique to hip OA patients when compared to knee OA and RA patients. The findings of this study offer a groundwork in tailoring novel targets and therapies for FAI and hip OA patients.
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3. ⭐ GSE326150 单细胞谱揭示化疗后肝母细胞瘤免疫细胞重塑和肿瘤-成纤维细胞相互作用增强

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、single-cell
• 📝 描述：Contributors : Rui Dong ; Deqian Chen ; Yong Zhan ; Jia Wang ; Kuiran DongSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHepatoblastoma (HB), the most common pediatric liver cancer, is typically treated with chemotherapy, yet its impact on the tumor microenvironment (TME) and mechanisms of chemoresistance remain unclear. We perform single-cell RNA sequencing on 32 HB tumors pre- and post-chemotherapy, integrating data from spatial transcriptomics, bulk transcriptomics, multiplexed immunofluorescence, and patient-derived xenografts. Chemotherapy enriches CD69⁺CD8⁺ T cells and shifted myeloid cells toward immune-activating phenotypes. HB tumor cells exhibit both hepatic and mesenchymal features, with hepatic-like cells showing greater chemoresistance. A subset of AFP-high hepatic tumor cells expresses high FGFR4 and showed elevated proliferation. Post-treatment, mesenchymal-like tumor cells and MMP11⁺ cancer-associated fibroblasts enhance FGF-FGFR signaling. FGFR4 inhibition significantly suppressed tumor growth in xenografts. These findings provide a high-resolution landscape of the HB immune TME and highlight cancer–fibroblast interactions, especially via FGF signaling, as key contributors to chemoresistance.
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4. ⭐ GSE294731 强效生物降解放线菌 Rhodococcus opacus 1CP：将芳香族化合物代谢与全基因组和转录组数据联系起来

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、genome、transcriptome
• 📝 描述：Contributors : Selvapravin Kumaran ; Thomas Heine ; Janosch A Gröning ; Tobias Busche ; Jörn Kalinowski ; Christian Rückert-Reed ; Michael Schlömann ; Dirk TischlerSeries Type : Expression profiling by high throughput sequencingOrganism : Rhodococcus opacusThe genus Rhodococcus comprises numerous strains recognized for pollutant degradation, secondary metabolite production including biosurfactant, lignin breakdown, or utilization of volatile organic compounds. Often gene redundancies and evolution of alternative pathways are attributed to such characteristics. Rhodococcus opacus 1CP initially isolated as a chlorophenol degrading strain was found to be a model organism comprising several such features. In this study, we analyzed the genome and transcriptome and demonstrated that the strain 1CP undergo three different routes of ortho, meta, and side chain attack in degrading aromatic compounds. The wild type strain, single or double knock-out mutant of phenol hydroxylases, well compensated the loss and chooses the classical ortho-route to attack substituted phenols, while the triple knock-out mutant takes the meta-pathway to act on p-cresol indicating that this pathway serves as a reserve in strain 1CP. Growth of 1CP in phenol, p-cresol and styrene induces several gene clusters that are associated in lignin metabolization. Catechol, protocatechuate, and phenylacetic acid are major key intermediates that are funneled into central pathways which enable the strain 1CP to degrade acetophenone, benzoate, phenol, 2-phenylethanol, and styrene. Strain 1CP has an alternative option with the modified ortho-cleavage pathway which enables it to degrade 2-chlorophenol. Interestingly, in almost all cases, redundant genes were identified, but only in minor cases as phenol hydroxylases, they were found to be active and simultaneously involved in metabolic activities. The transcriptome and kinetic data showed that the redundant styrene-oxide isomerase is upregulated and involved in styrene degradation.
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5. ⭐ GSE289672 单细胞转录组学揭示肾髓质癌与透明细胞肾细胞癌不同的生物学和免疫代谢特征

• ✍️ 作者：未知作者
• 🏷️ 关键词：carcinoma、single-cell、transcriptomics
• 📝 描述：Contributors : Xinmiao Yan ; Jianfeng Chen ; Jianjun Gao ; Linghua Wang ; Pavlos MsaouelSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensRenal medullary carcinoma (RMC) is a rare, highly aggressive kidney malignancy primarily affecting young individuals of African descent with sickle cell trait. The currently available targeted therapies and immunotherapies approved for clear cell renal cell carcinoma (ccRCC) are ineffective against RMC, highlighting the urgent need for novel treatment approaches specifically tailored to the distinct biological and immune hallmarks of RMC. Here, we performed single-cell RNA-sequencing (scRNA-seq) of tumor samples from five patients with RMC and five patients with ccRCC to define their immunometabolic and transcriptomic landscapes. Differential expression analysis identified ENPP3 and CA9 as distinct cell surface markers upregulated in ccRCC, whereas MUC16, TROP2, and EPCAM were upregulated in RMC tumors cells. RMC displayed a more immunosuppressive tumor microenvironment (TME), with lower infiltration of T and NK cells but an enrichment of immunosuppressive SPP1+ macrophages, contrasting with the more immune-rich TME in ccRCC. Ligand-receptor interaction analyses revealed stronger VEGF-VEGFR signaling in ccRCC and enhanced APP-CD74 signaling in RMC. Nephron anatomy mapping indicated that RMC originates in the loop of Henle, whereas ccRCC arises from proximal tubule cells. We uncovered distinct metabolic reprogramming, with RMC demonstrating higher oxidative phosphorylation (OXPHOS) and lower glycolysis compared to ccRCC. These findings were validated in vitro with RMC cell lines showing elevated oxygen consumption and diminished extracellular acidification compared with ccRCC cell lines. Overall, this study underscores the distinct origins, gene expression patterns, and immunometabolic features of RMC versus ccRCC, offering insights for future tailored therapeutic strategies against RMC.
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6. GSE319646 scRNA测序揭示了HIV相关的炎症介导的肺上皮功能紊乱和成纤维细胞重塑

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、scRNA
• 📝 描述：Contributors : Khursheed Ul Islam ; Gagandeep Kaur ; Sadiya Bi Shaikh ; Kingshuk Panda ; Srinivasan Chinnapaiyan ; Hoshang Unwalla ; Irfan RahmanSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHIV infection is a well-recognized risk factor for a wide spectrum of pulmonary diseases, with incidence rates significantly higher in people living with HIV (PLWH). Despite antiretroviral therapy, persistent immune activation and recurrent injury continue to compromise lung integrity in this population. However, the mechanism through which HIV disrupts alveolar homeostasis and reshapes epithelial, immune, and stromal compartments in the lungs remain poorly defined. To characterize the cellular and molecular landscape of HIV infection within the lungs upon tobacco smoking, we performed single cell RNA sequencing (scRNA-seq) on human lung tissues from HIV non-smokers and smokers compared them with HIV positive subjects with and without a smoking history. Integration and Uniform Manifold Approximation and Projection (UMAP) clustering of 54,320 cells from all experimental groups identified 29 transcriptionally distinct clusters upon scRNA seq analyses. HIV infection profoundly altered lung cellular composition, marked by expansion of CD4+, CD8+ T-cells, B cells, and non-classical monocytes, alongside reduced fibroblast abundance. Alveolar Type I and Type II epithelial cells displayed robust HIV-associated transcriptional reprogramming. In AT1 cells,. Fibroblast and smooth muscle cells showed enhanced proinflammatory and stress responsiveness with suppression of extracellular matrix and contractile programs. EMT marker analysis revealed cell type specific shifts with: (a) AT1 cells exhibiting reduced E-cadherin and increased vimentin gene expression, (b) AT2 cells adopting a hybrid epithelial mesenchymal phenotype, and (c) myofibroblast cluster displaying amplified mesenchymal activation. These findings reveal HIV as a potent driver of epithelial dysregulation in the human lung, and suggest that targeting epithelial stress programs and fibroblast remodeling may offer new therapeutic avenues, supporting future efforts to develop therapeutic interventions tailored for PLWH.
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7. GSE295293 肝纤维化进展和消退的单细胞固定RNA测序

• ✍️ 作者：未知作者
• 🏷️ 关键词：RNAseq、single-cell
• 📝 描述：Contributors : Duc M Pham ; Thuy T Le ; Norifumi KawadaSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusLiver fibrosis regression is a dynamic process involving a variety of hepatic and immune cell populations. Using single-cell fixed RNA profiling (FLEX) on mouse livers from control, TAA-induced cirrhotic, and regression phases, we analyzed 38,136 cells across 10 major cell types. Regression was characterized by the emergence of pericentral hepatocytes enriched in detoxification and antioxidant genes (e.g., Cyp2e1, Txn1), which secreted RARRES2 to modulate hepatic stellate cells (HSCs). Recovered liver sinusoidal endothelial cells (LSECs) expressed scar-resolving genes (Mmp14, Ctsl) and restored fenestrae structure. Kupffer cells regained anti-inflammatory phenotypes, while SEMA4D, produced by monocyte-derived macrophages, activated HSCs; blockade of SEMA4D reduced fibrosis in vivo. Fibrogenic cholangiocyte subsets and LMCD1⁺ HSCs were diminished during regression, with LMCD1 identified as a novel marker of HSC activation. Additionally, NK/T cells, B cells, and neutrophils displayed recovery-associated transcriptional signatures. This single-cell atlas uncovers key transcriptional programs and intercellular interactions driving fibrosis resolution and highlights potential therapeutic targets for chronic liver disease.
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8. GSE281245 单细胞 RNA 测序鉴定出马兜铃酸 I (AAI) 诱导的 AKI 向 CKD 转变小鼠模型中独特的巨噬细胞群

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing、single-cell
• 📝 描述：Contributors : Xiangchen Gu ; Chenxi Wang ; Lin Xie ; Yaodong Gu ; Min ChenSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusAcute Kidney Injury (AKI) often progresses to Chronic Kidney Disease (CKD), resulting in significant morbidity and mortality. The transition from AKI to CKD is driven by complex cellular mechanisms that are not yet fully understood. In this study, we used an Aristolochic Acid I (AAI)-induced murine model to investigate these mechanisms, performing single-cell RNA sequencing (scRNA-seq) to comprehensively profile kidney immune cells during the AKI to CKD transition. Our analysis revealed significant changes in immune cell populations, particularly macrophages and T lymphocytes. We identified a novel subpopulation of macrophages characterized by the expression of Ctsk, Mmp9, and Acp5, which emerged during the CKD phase. These macrophages were found to interact with T cells, injured proximal tubules, and fibroblasts, suggesting their involvement in chronic inflammation and fibrosis. Targeting this specific macrophage subpopulation may represent a potential therapeutic approach to prevent CKD progression. Additionally, T lymphocytes underwent a transition from effector to exhausted phenotypes, indicating chronic immune activation and sustained inflammation in CKD. Our findings provide new insights into the immune landscape of kidney injury and highlight potential targets for therapeutic intervention in preventing the progression from AKI to CKD.
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9. GSE277625 H2O2 诱导的星形胶质细胞胶原蛋白触发缺血性中风中的神经元死亡 [ATAC-seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：Neuronal、ATAC-seq
• 📝 描述：Contributors : In Y Hwang ; Jae H Lee ; C J LeeSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusIschemic stroke is a brain injury caused by the occlusion of blood vessels, leading to reduced blood flow, excessive oxidative stress, and the cascade of events, including the formation of the glial barrier, fibrotic scar, neuronal death, and motor impairment. Despite extensive research into stroke etiology, the specific initiation trigger for neuronal death is mainly unknown, severely limiting the development of effective treatments. Here, we demonstrate that excessive H2O2 generation is the initiating factor of ischemic stroke in the photo-thrombosis (PT) mouse and non-human primate (NHP) models, with H2O2-induced astrocytic type I collagen (COL1) playing a crucial role in the cascade of stroke pathology. Treatment with KDS12025, an H2O2-decomposing peroxidase enhancer, significantly alleviates these effects by reducing H2O2-induced COL1 in extremely low doses in mouse and NHP stroke models. In cultured astrocytes, H2O2 stimulates the production of astrocytic COL1 through post-transcriptional up-regulation of Col1 mRNA by decreasing microRNA29, leading to the death of neighboring neurons. Using matrix-assisted laser desorption/ionization mass spectrometry imaging (MALDI-MSI), we observe profound alterations in N-glycan profiles, particularly fucosylated N-glycans, which reverted to normal levels in both the KDS12025 treatment and astrocytic Col1 gene-silencing groups. The gene-silencing of astrocytic Col1 or Fut8, a key enzyme responsible for core fucosylation necessary for COL1 secretion, prevents neuronal death and motor impairment. Our findings reveal that H2O2-induced astrocytic COL1 production is critical to ischemic stroke. These findings propose that targeting H2O2, astrocytic COL1, and FUT8 could be effective therapeutic strategies for ischemic stroke, offering new avenues for treatment.
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10. GSE325769 使用 SEPARATE-Seq 对患者相关的原位肺癌模型进行多组学免疫分析 [MERSCOPE]

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer、immune
• 📝 描述：Contributors : Daliya Kancheva ; Pauline Bardet ; Lize Allonsius ; Eva Hadadi ; Damya LaouiSeries Type : OtherOrganism : Mus musculus ; synthetic constructRelevant pre-clinical models are essential for driving progress in cancer therapy research. Here, we developed a pre-clinical study framework using an injectable orthotopic lung adenocarcinoma (LUAD) model (ORTHO) that replicates key features of human LUAD patients and is dissectible into tumoural and non-tumoural adjacent tissue, in analogy with patient samples. We also present SEPARATE-Seq, a technique enabling the partitioning of vascular and intratissue immune cells along with scRNA-Seq. By applying both SEPARATE-Seq and spatial transcriptomics to our dissectible ORTHO model, we confirmed that our model replicates key immune features of human LUAD patients. Similarly to these patients, we observed NK-cell dysfunction and neutrophil dichotomy, and uncovered that these are driven by their vascular/intratissue or tumour/adjacent location, highlighting the need for these spatial distinctions. Additionally, we reveal that several immune populations are restricted to specialised, local niches within the tumour, including a ring of lipid-associated TAMs lining the tumour edge and hubs of interferon-stimulated cells. Overall, our resource, available through an interactive tool, provides a comprehensive multiomics immune characterisation of a reproducible pre-clinical LUAD mouse model.
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详细内容（全部3条）

1. ⭐ 科学家发现肠道细菌会注入控制免疫系统的蛋白质。

• ✍️ 作者：未知作者
• 🏷️ 关键词：immune、bacteria、regex:bacter(ia|ial|ium)、gut、regex:gut(-?microbiome)?
• 📝 描述：Gut bacteria aren’t just passive passengers—they can actively send proteins straight into our cells. Using microscopic injection systems, even harmless microbes can influence immune responses and metabolic pathways. Researchers found these interactions may play a role in inflammatory diseases like Crohn’s. It’s a major shift in how scientists understand the microbiome’s power over human health.
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2. 利用长读长测序对环状RNA检测进行基准测试

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：Long-read RNA sequencing improves circular RNA detection, revealing tool differences and highlighting the need for combined approaches to better interpret RNA sequencing data..
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3. 科学家发现癌症药物并非对所有人有效的原因

• ✍️ 作者：未知作者
• 🏷️ 关键词：cancer
• 📝 描述：Scientists have uncovered a hidden reason why cancer treatments don’t work equally well for everyone. Certain drugs can become trapped inside lysosomes within tumor cells, forming slow-release reservoirs that create uneven drug distribution. This means some cancer cells are heavily exposed while others are barely affected. Understanding this process could help doctors better tailor treatments and improve outcomes.
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• GSE318191 研究发现，休眠状态的解除与 Creb1 的重新激活相关，而 Creb1 是克服 ER+ 乳腺癌细胞内分泌治疗耐药性的潜在靶点。
• GSE301089 核特异性还原羧化α-酮戊二酸促进组蛋白乙酰化，从而诱导FOXA1依赖性基因激活[RNA-seq]
• GSE288240 组蛋白去乙酰化酶活性并非 HDAC 抑制剂的普遍抗癌靶点 [RNA-seq_MC38]
• GSE293303 细胞周期重编程介导胰腺癌获得性奥沙利铂耐药性。
• GSE322522 心脏手术患者左心耳RNA测序：微（纳米）塑料负荷高低对比的心脏手术患者
• GSE325636 细菌对环境信号响应分析框架：沙门氏菌对19种宿主相关分子的响应
• GSE325168 碱基编辑恢复了 CDKL5 表达，并挽救了 CDKL5 缺乏症患者模型中的神经元缺陷
• GSE326189 染色质结构的改变以 DUX 依赖的方式促进全能性样特征 [ChIP-seq]
• GSE317634 核受体 REV-ERBβ 对 TH17 介导的炎症的负调控
• GSE315712 前节发育的单细胞表征：驱动小梁网和施莱姆氏管形成的细胞类型、通路和信号
• GSE307092 IL-36γ 装甲 CAR T 细胞重编程中性粒细胞以诱导内源性抗肿瘤免疫
• GSE301095 α-酮戊二酸的核特异性还原羧化促进组蛋白乙酰化，从而诱导 FOXA1 依赖性基因激活 [MB-231 ATAC]
• GSE301090 α-酮戊二酸的核特异性还原羧化促进组蛋白乙酰化，从而诱导 FOXA1 依赖性基因激活 [C42_ATAC]
• GSE289305 染色质结构的改变以 DUX 依赖的方式促进全能性样特征 [RNA-Seq]
• GSE289302 染色质结构的改变以 DUX 依赖的方式促进全能性样特征 [ATAC-Seq]
• GSE285077 染色质相关 lncRNA 剪接因子凝聚体调节核斑点附近预定位基因的缺氧反应 RNA 加工 [RNA-seq]
• GSE242214 脑神经血管相互作用的分子图谱揭示了 TGFβ 信号在脑血管生成中的时空需求 [Visium]
• GSE242213 脑神经血管相互作用的分子图谱揭示了 TGFβ 信号在脑血管生成中的时空需求 [scRNA-seq]
• GSE325800 KMT2C 和 KMT2D 增强 GRHL2 驱动的增强子激活 [RNA-Seq]
• GSE325729 人类健康供体中 SIT1 敲除和对照 T 细胞的批量 RNA 测序
• GSE298652 小胶质细胞IL-27调节出生后免疫激活诱发的抑郁症状
• GSE293271 阿贝西利增强达沙替尼在乳头状肾细胞癌中的抗肿瘤活性
• GSE262776 IRX3 的缺失促进人类 Ipsc 衍生心肌细胞的早期心脏定向分化和成熟
• GSE262722 siRNA敲低Agrin后BJ细胞的转录组分析。
• GSE322523 异丙肾上腺素（ISO）损伤模型中小鼠心脏RNA测序，伴或不伴聚苯乙烯纳米塑料共同暴露