科研日报 2026-04-06
📅 Daily Report - 2026-04-06
今日筛选出 14 条内容,来自 2 个来源
🤖 今日AI智能总结
🧬 数据前沿
今日焦点: GSE326538研究发现,艾叶水提物通过调控肠道菌群、代谢稳态及肺部炎症信号,有效缓解急性肺损伤。GSE228952揭示了人膀胱癌组织与癌旁正常组织在表观遗传层面的差异。
主要方向:
- 肿瘤微环境与免疫应答:GSE305407关注GPR35+肿瘤相关中性粒细胞在肝癌中的促瘤作用;GSE325273探究4-1BBL对巨噬细胞代谢重塑影响的抗炎反应调控。
- 代谢性疾病与信号通路:GSE326605发现胆酸摄取激活STAT信号并损害NK细胞功能,与代谢功能障碍相关性脂肪性肝炎相关。
- 表观遗传与基因调控:GSE293892显示HDAC5缺陷通过干扰c-Myc乙酰化-泛素化稳态,诱导对KRASG12D抑制的内在抵抗;GSE291274和GSE229172分析了不同发育阶段视网膜类器官的转录组以及BLACAT3敲低对膀胱癌细胞的影响。
技术亮点:
- 多组学整合分析:GSE228952结合了甲基化、基因表达和非编码RNA测序,全面解析膀胱癌的表观遗传特征。
- 高通量测序技术:多项研究(如GSE326538, GSE305407, GSE325273, GSE326605, GSE326554, GSE293892, GSE291274, GSE264235, GSE264234, GSE229172, GSE301123)广泛应用高通量测序,为大规模基因组学和转录组学研究提供了基础。
🧪 博客更新
今日焦点: 人工智能辅助肠道菌群与代谢物分析,有望实现消化道疾病早期精准检测;新型“智能”DNA药物实现对癌细胞的超高精度靶向。
主要方向:
- 利用AI分析肠道生物标志物,实现消化道疾病(如一种特定疾病)的早期筛查。
- 开发基于合成DNA的靶向药物,精准识别并激活,特异性杀伤癌细胞。
技术亮点:
- AI在肠道微生物组和代谢物数据分析中的应用。
- 可编程DNA药物设计,通过特定肿瘤标志物组合触发。
📚 分类浏览
🧬 数据前沿 (12条)
详细内容(前10条)
1. ⭐ GSE326538 艾蒿水提取物通过协调肠道菌群、代谢稳态和肺部炎症信号传导来减轻急性肺损伤
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic、gut、regex:gut(-?microbiome)?
- 📝 描述:Contributors : Huixiang Wang ; Haihong JiaoSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBackground: Artemisia argyi is a traditional medicinal herb with established anti-inflammatory and immunomodulatory properties. Its aqueous extract (AEAA), enriched in water-soluble bioactive constituents, exhibits favorable safety and bioavailability; however, its potential protective effects against acute lung injury (ALI) and its associations with systemic immunometabolic regulation remain incompletely understood. Methods: An LPS-induced ALI mouse model was established following 28 days of AEAA pretreatment. Lung histopathology, pulmonary edema, and inflammatory cytokines were evaluated. Integrated multi-omics analyses—including gut microbiota profiling, untargeted metabolomics of colonic contents and serum, and lung transcriptomics—were performed to characterize treatment-associated microbial, metabolic, and transcriptional alterations.Results: Lung transcriptomic profiling suggested attenuation of LPS-associated transcriptional signatures related to NF-κB, MAPK, Toll-like receptor, and PI3K–AKT signaling pathways. Cross-omics integration further revealed coordinated associations among microbial shifts, metabolic remodeling, and pulmonary inflammatory gene expression.Conclusion: These findings suggest that aqueous Artemisia argyi extract is associated with mitigation of LPS-induced acute lung injury, accompanied by coordinated alterations in gut microbiota composition, host metabolic profiles, and pulmonary inflammatory gene expression. Although causal relationships were not established, this integrated multi-omics analysis provides a systems-level, hypothesis-generating framework supporting the potential of AEAA as a multi-target botanical candidate for ALI.
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2. GSE305407 GPR35+肿瘤相关中性粒细胞促进肝细胞癌的肿瘤生长。
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、carcinoma
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusBulk RNA-seq profiling of tumor-associated neutrophils from Hepa1-6 mouse hepatocellular carcinoma (HCC) models. Neutrophils were isolated from mice HCC tissues and classified as GPR35+ or GPR35- subsets (n=3 per group). Differential expression analysis revealed significant upregulation of MAPK signaling pathway and pathways associated with neutrophil migration and cytokines production in GPR35+ neutrophils. These data support the pro-tumorigenic role of GPR35+ neutrophils in HCC.
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3. GSE228952 人类膀胱癌组织:肿瘤与邻近正常组织对比
- ✍️ 作者:未知作者
- 🏷️ 关键词:tumor、cancer
- 📝 描述:Contributors : Jinbo Xie ; Bo PengSeries Type : Methylation profiling by array ; Expression profiling by array ; Non-coding RNA profiling by arrayOrganism : Homo sapiensm6A Epitranscriptomic Microarray nanlysis was conducted to investigate m6A methylation level and expression level profiling of the lncRNAs between bladder cancer tissues and adjacent normal tissues.
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4. GSE325273 4-1BBL 通过调节巨噬细胞的代谢重编程来抑制抗炎反应的诱导
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic
- 📝 描述:Contributor : Young Jun KangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusIntegration of intracellular signaling and metabolic reprogramming is critical for macrophage polarization and the induction of pro- or anti-inflammatory responses. However, the molecular switches that govern macrophage polarization remain incompletely defined. While 4-1BB ligand (4-1BBL), a member of the TNF superfamily, is known to promote sustained pro-inflammatory responses in macrophages, its role in anti-inflammatory macrophage responses has not been elucidated. This study identifies 4-1BBL plays a role as a negative regulator of anti-inflammatory macrophage polarization. Genetic deletion or pharmacological inhibition of 4-1BBL significantly enhanced the expression of anti-inflammatory cytokines and markers in mouse macrophages. In IL-4R signaling, 4-1BBL restrained JAK1 (Janus kinase 1) and STAT (signal transducer and activator of transcription) 6 phosphorylation, thereby modulating transcriptional programs associated with anti-inflammatory macrophage activation. Consistently, 4-1BBL deficiency elevated mitochondrial oxidative phosphorylation and fatty acid oxidation, accompanied by increased expression of metabolic genes in anti-inflammatory macrophages. Transcriptomic analysis further revealed a shift toward anti-inflammatory and oxidative metabolic gene signatures in IL-4-treated 4-1BBL-deficient macrophages. Importantly, inhibition of 4-1BBL signaling also augmented anti-inflammatory responses in human monocytes and facilitated the transition from pro-inflammatory to anti-inflammatory phenotypes. Collectively, these findings establish 4-1BBL as a molecular switch that regulates macrophage polarization by integrating inflammatory signaling with metabolic reprogramming, highlighting 4-1BBL as a potential therapeutic target for promoting inflammation resolution.
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5. GSE326605 胆汁酸摄取激活STAT信号通路并损害代谢功能障碍相关性脂肪性肝炎中的自然杀伤细胞
- ✍️ 作者:未知作者
- 🏷️ 关键词:metabolic
- 📝 描述:Contributors : Ahmad Salhab ; Johnny Amer ; Lu Yinying ; Rifaat SafadiSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensMetabolic dysfunction-associated steatotic liver disease (MASLD) encompasses a spectrum of fatty liver diseases ranging from steatotic liver disease to metabolic dysfunction-associated steatohepatitis (MASH), and its prevalence is increasing worldwide due to the pandemic of obesity. Approximately 20–30% of MASLD patients develop MASH, leading to liver cirrhosis and associated complications, including hepatocellular carcinoma. Liver damage, such as cholestatic conditions in which bile secretion and flow are disturbed, is associated with impaired innate and adaptive immunity. NK cells play a crucial role in inhibiting liver fibrosis. However, how bile acids affect natural killer (NK) cells remains unknown. We aimed to assess the impact of bile acid concentration on NK cell functionality and identify the molecular and metabolic NK cell signaling pathways that influence liver fibrosis pathogenesis. To this end, we studied peripheral NK cells from patients with MASH, healthy donors, and a mouse model of MASH. Sodium+/taurocholate cotransporting polypeptide (NTCP) expression was 2.5-fold higher in peripheral blood NK cells from MASH patients with advanced liver fibrosis than in those from early liver fibrosis patients and healthy donors. Greater taurocholic acid (TCA) uptake was observed in peripheral NKNTCP+ cells from the early and advanced liver fibrosis MASH patient groups than in NKNTCP- cells from the same patients. It was associated with increased levels of exhaustion markers and decreased activity. Moreover, single-cell RNA sequencing and functional analyses demonstrated that NTCP⁺ NK cells in advanced MASH adopt stress- and exhaustion-associated transcriptional programs with reduced translational activity, accompanied by increased STAT3 activation and diminished STAT1 signaling, highlighting their impaired cytotoxic function. Following STAT3 inhibition, trNKNTCP+ cells presented significantly reduced NTCP expression, reduced NK cell exhaustion, and restored NK cell activity. In MASH mice, epigallocatechin gallate-mediated inhibition of NTCP expression reduced TCA uptake and attenuated liver fibrosis. Additionally, in immunodeficient liver fibrosis model mice, reconstitution with trNKNTCP- cells alleviated liver fibrosis, decreased proinflammatory and profibrotic cytokine levels, and ameliorated lipi…
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6. GSE326554 不同发育阶段野生型人iPSC衍生视网膜类器官的RNA测序
- ✍️ 作者:未知作者
- 🏷️ 关键词:RNA-seq
- 📝 描述:Contributors : Srishti Silvano ; Rick-Lenze van Annika ; Jacob Sampson ; Milena Zitnik-Sergeant ; Jamie Ellingford ; Manning CerysSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensHuman retinal organoids derived from pluripotent stem cells provide an in vitro system to model key aspects of early human retinal development and to investigate mechanisms underlying developmental eye disorders. Congenital eye diseases, such as microphthalmia, anophthalmia and coloboma, arise from disruptions in gene regulatory programs that control retinal progenitor specification and neuronal differentiation. However, studying these processes in humans is challenging due to limited access to developing retinal tissue.Here we present a temporal bulk RNA sequencing dataset of retinal organoids collected across multiple stages of differentiation (days 0, 35, 60, 90, 120, and 150). These timepoints span early retinal lineage specification through progressive neuronal differentiation and maturation of retinal cell types. The dataset captures dynamic gene expression changes associated with retinal development and provides a transcriptional framework for studying genes implicated in congenital and developmental retinal disorders.
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7. GSE293892 HDAC5 缺陷通过破坏 c-Myc 乙酰化-泛素化稳态诱导对 KRASG12D 抑制的内在耐药性
- ✍️ 作者:未知作者
- 🏷️ 关键词:resistance
- 📝 描述:Contributors : Zhou Yingke ; Yu HaixinSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensWe found that HDAC5 deletion significantly enhances intrinsic resistance to MRTX1133 in KRASG12D mutant pancreatic cancer. Mechanistic studies show that HDAC5 deletion promotes resistance to KRASG12D inhibitors by sustaining the activation of the MAPK signaling pathway.
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8. GSE291274 胎盘特异性组蛋白H3.4促进生殖细胞发育和生殖能力
- ✍️ 作者:未知作者
- 🏷️ 关键词:histone
- 📝 描述:Series Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusThis SuperSeries is composed of the SubSeries listed below.
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9. GSE264235 假手术、心肌梗死损伤和 FGF17 治疗的心肌梗死小鼠心脏的转录组分析(正常)
- ✍️ 作者:未知作者
- 🏷️ 关键词:transcriptome
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThis study investigated whether FGF17 signaling exerts cardioprotective effects in un-injured normal mice hearts.
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10. GSE264234 假手术、MI损伤和FGF17治疗的MI小鼠心脏的转录组分析(MI)
- ✍️ 作者:未知作者
- 🏷️ 关键词:transcriptome
- 📝 描述:Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusFibroblast growth factor (FGF) signal transduction plays essential roles in cardiac repair following myocardial infarction (MI). Among which, FGF17 was demonstrated to regulate epicardial epithelial-mesenchymal transition to provide new vasculature for muscle regeneration during the process of myocardial repair in zebrafish. However, little is known about its function in the mammalian cardiovascular system. This study investigated whether FGF17 signaling exerts cardioprotective effects in ischemic mice hearts, and attempted to elucidate the underlying mechanisms.
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💡 该来源还有 2 条内容,详见 文末
🧪 博客更新 (2条)
详细内容(全部2条)
1. ⭐ 科学家发现隐藏的肠道信号,或可早期检测癌症。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer、gut、regex:gut(-?microbiome)?
- 📝 描述:A new study reveals that gut bacteria and metabolites may hold the key to detecting serious digestive diseases earlier and more easily. Using AI, scientists found that biomarkers linked to one condition can often predict others, showing these diseases are more interconnected than previously thought. This cross-disease insight could lead to faster diagnoses without invasive procedures.
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2. 科学家研发出一种“智能”DNA药物,能够极其精准地靶向癌细胞。
- ✍️ 作者:未知作者
- 🏷️ 关键词:cancer
- 📝 描述:Scientists have created a programmable drug system that can zero in on cancer cells with unprecedented accuracy. Built from synthetic DNA, it only activates when it detects a precise combination of tumor markers, preventing damage to healthy tissue. The system can also deliver multiple drugs at once, potentially overcoming resistance. This marks a step toward medicines that behave more like smart, responsive machines inside the body.
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📊 关键词统计
| 关键词 | 出现次数 |
|---|---|
| cancer | 4 |
| metabolic | 4 |
| gut | 2 |
| regex:gut(-?microbiome)? | 2 |
| tumor | 2 |
| transcriptome | 2 |
| RNA-seq | 1 |
| carcinoma | 1 |
| resistance | 1 |
| histone | 1 |
📎 更多内容
📅 报告生成时间:2026-04-05 21:52
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