详细内容（前10条）

1. ⭐ GSE331083 CCR5 hi 单核细胞的代谢-表观遗传重编程维持对致命性脓毒症的长期训练免疫力 [bulk RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、metabolic、RNA-seq、epigenetic
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusTrained immunity enhances innate host defense by endowing monocytes with memory-like properties, yet the underlying integrated metabolic and epigenetic mechanisms remain elusive. Here, we demonstrate that co-immunization with Bacillus Calmette–Guérin (BCG) and bacterial lipoprotein (BLP) induces a durable form of trained immunity that provides robust, long-term protection against polymicrobial sepsis from early life into adulthood. Single-cell RNA sequencing revealed that this effect is mediated by an expansion of CCR5hi memory-like monocytes with enhanced antimicrobial capacity. Mechanistically, BCG+BLP vaccination activated the AKT–mTOR–HIF-1α axis, driving glycolytic reprogramming and subsequent lactate accumulation. We found that elevated lactate then promoted KAT2B-dependent histone H3K18 lactylation, an epigenetic mark directly facilitating the transcription of phagocytic and inflammatory genes. Critically, CCR5hi monocytes isolated from vaccinated human cord blood recapitulated these lactate-driven lactylation and trained immunity features. Together, our findings define a novel lactate–KAT2B–H3K18la epigenetic axis that orchestrates the long-term reprogramming of CCR5hi monocytes, highlighting CCR5hi monocytes as a promising therapeutic target for modulating innate immunity against lethal sepsis
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2. ⭐ GSE310218 膳食蛋氨酸限制可促进T细胞代谢活化和肿瘤抑制，并增强免疫检查点阻断的疗效

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、immune、T cell、metabolism
• 📝 描述：Series Type : Expression profiling by high throughput sequencingOrganism : Mus musculusThe proliferation of many cancer cells is methionine dependent and dietary methionine restriction (MR) has shown anti-tumor effects in a wide variety of immunodeficiency preclinical models. Yet, whether MR exerts an anti-tumor effect in the presence of an immune-competent background remains inconclusive. Accumulating evidence has shown an essential role of methionine in immune cell differentiation and function. Thus, competition for methionine between tumor cells and immune cells in the tumor microenvironment may drive tumor growth and tumor response to therapy. Here, we aim to define the impact of MR on tumor growth and associated immunity. We first assessed the effect of MR in a series of immunocompetent mouse models of melanoma, colorectal cancer, breast cancer, and lung. MR led to a broad tumor inhibition effect across these models and such tumor inhibition was not sex- or genetic background-dependent but appears to be fully or partially immune-dependent. Through flow cytometry analysis, we found a consistent increase in intratumoral activated CD8+ T cells across different tumor models and depletion of CD8+ T cells partially or completely reversed MR-induced tumor inhibition in a model dependent manner. Interestingly in young healthy non-tumor-bearing mice, MR increased spleen CD3+ and CD8+ T cell populations. Metabolomics and RNAseq analysis of spleen-derived CD8+ T cells revealed significant increase in purine metabolism and amino acid metabolism and that are in line with the metabolic feature of activated T cells. Furthermore, MR improved the efficacy of anti-PD1 immune checkpoint blockade. Together, MR primes T cell metabolism for its anti-tumor effect and improves the efficacy of anti-PD1 checkpoint blockade.
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3. ⭐ GSE284278 中性粒细胞与上皮样癌细胞的共生粘附塑造肿瘤微环境并促进转移[2]

• ✍️ 作者：未知作者
• 🏷️ 关键词：tumor、cancer、tumor microenvironment
• 📝 描述：Contributors : Ling Wu ; Xiang ZhangSeries Type : Expression profiling by high throughput sequencingOrganism : Mus musculusNeutrophils play complicated roles in tumor progression. Examination of several murine triple negative breast cancer (TNBC) models revealed nearly opposite impact of neutrophils on epithelial-like vs. mesenchymal-like cancer cells (ECCs vs. MCCs). Interaction with ECCs upregulates ICAM1 in neutrophils, a feature that also distinguishes tumor-infiltrating neutrophils from other neutrophils in human. Direct adhesion between ECCs and neutrophils, especially the ICAMhigh subpopulation, promote the survival of each other – forming a symbiotic relationship. In contrast, MCCs are thwarted by neutrophils due to decreased cell adhesion and elastase resistance. The ICAM1high neutrophils are known for reverse migration to circulation. The adhesive and reverse migratory properties of ICAM1high neutrophils mediate intravasation of metastatic seeds. These observations were verified in a subset of human TNBCs that unexpectedly enrich non-Hispanic European patients. Thus, we demonstrated a co-evolution through which neutrophils sculpt phenotypes and metastatic behaviors of TNBC, which may preferentially occur in patients of certain race/ethnicity.
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4. ⭐ GSE279411 线粒体代谢和表观遗传串扰驱动SASP（RNA-Seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、RNA-seq、epigenetic
• 📝 描述：Contributors : Helene Martini ; João F PassosSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSenescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.
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5. ⭐ GSE279410 线粒体代谢和表观遗传串扰驱动SASP（ChIP-seq）

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、ChIP-seq、epigenetic
• 📝 描述：Contributors : Helene Martini ; Aaron Havas ; Rabi Murad ; Xue Lei ; Rebecca A Porritt ; Peter D Adams ; João F PassosSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSenescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.
• 🔗 查看原文

6. ⭐ GSE331085 CCR5 hi 单核细胞的代谢-表观遗传重编程维持对致命性脓毒症的长期训练免疫力 [CUT&Tag]

• ✍️ 作者：未知作者
• 🏷️ 关键词：immunity、metabolic、epigenetic
• 📝 描述：Series Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusTrained immunity enhances innate host defense by endowing monocytes with memory-like properties, yet the underlying integrated metabolic and epigenetic mechanisms remain elusive. Here, we demonstrate that co-immunization with Bacillus Calmette–Guérin (BCG) and bacterial lipoprotein (BLP) induces a durable form of trained immunity that provides robust, long-term protection against polymicrobial sepsis from early life into adulthood. Single-cell RNA sequencing revealed that this effect is mediated by an expansion of CCR5hi memory-like monocytes with enhanced antimicrobial capacity. Mechanistically, BCG+BLP vaccination activated the AKT–mTOR–HIF-1α axis, driving glycolytic reprogramming and subsequent lactate accumulation. We found that elevated lactate then promoted KAT2B-dependent histone H3K18 lactylation, an epigenetic mark directly facilitating the transcription of phagocytic and inflammatory genes. Critically, CCR5hi monocytes isolated from vaccinated human cord blood recapitulated these lactate-driven lactylation and trained immunity features. Together, our findings define a novel lactate–KAT2B–H3K18la epigenetic axis that orchestrates the long-term reprogramming of CCR5hi monocytes, highlighting CCR5hi monocytes as a promising therapeutic target for modulating innate immunity against lethal sepsis
• 🔗 查看原文

7. GSE326624 线粒体代谢和表观遗传串扰驱动 SASP (ChIP-seq_2)

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、epigenetic
• 📝 描述：Contributors : Helene Martini ; Joao F Passos ; Rabi Murad ; Xue Lei ; Peter D AdamsSeries Type : Genome binding/occupancy profiling by high throughput sequencingOrganism : Homo sapiensSenescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.
• 🔗 查看原文

8. GSE324238 线粒体代谢和表观遗传串扰驱动SASP（多组）

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、epigenetic
• 📝 描述：Contributors : Helene Martini ; Joao F Passos ; Wazim Mohammed Ismail ; Alexandre Gaspar-MaiaSeries Type : Expression profiling by high throughput sequencing ; Genome binding/occupancy profiling by high throughput sequencingOrganism : Mus musculusSenescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.
• 🔗 查看原文

9. GSE319937 线粒体代谢和表观遗传串扰驱动 SASP (RNA-Seq_2)

• ✍️ 作者：未知作者
• 🏷️ 关键词：metabolism、epigenetic
• 📝 描述：Contributors : Helene Martini ; Joao F PassosSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensSenescent cells drive age-related tissue dysfunction largely through the persistent activation of the senescence-associated secretory phenotype (SASP). Here, we identify key mitochondrial metabolic pathways, including the mitochondrial citrate carrier (SLC25A1) and ATP-citrate lyase (ACLY), as critical regulators of the SASP. These pathways fuel histone acetylation at SASP gene loci, promoting their expression. Targeted inhibition of SLC25A1 or ACLY suppresses SASP expression without affecting cell cycle arrest, underscoring their potential as selective therapeutic targets for mitigating age-related inflammation. Furthermore, pharmacological inhibition of SLC25A1 reduces systemic inflammation and extends healthspan in aged mice. Our findings suggest that disrupting metabolic reprogramming in senescent cells offers a promising strategy to ameliorate aging-associated pathologies.
• 🔗 查看原文

10. GSE297397 白血病风险因子 ARID5B 协调 HDAC 介导的转录抑制 [RNA-Seq]

• ✍️ 作者：未知作者
• 🏷️ 关键词：leukemia、RNA-seq
• 📝 描述：Contributors : Ana P Kutschat ; Sophie Müller ; Davide SeruggiaSeries Type : Expression profiling by high throughput sequencingOrganism : Homo sapiensWe employed a combination of proteomics, genomics and transcriptomics to describe the molecular mechanisms of ARID5B. We identify that ARID5B interacts with MIER1, C16ORF87, HDAC1 and HDAC2 forming a repressor complex. The former localizes to active regions of the genome, tethering HDAC1 and HDAC2 to enhancers and promoters. Genes actively repressed by the ARID5B repressor complex are involved in B cell-specific signaling.
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1. 血液RNA测序检测有助于预测疾病进展和治疗效果。

• ✍️ 作者：未知作者
• 🏷️ 关键词：sequencing
• 📝 描述：RNA sequencing combined with RNA velocity enabled prediction of disease progression, treatment response, and clinical outcomes using whole-blood gene expression patterns…
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2. 最新研究揭示肥胖如何改变大脑脂质，从而加速阿尔茨海默病的发展进程。

• ✍️ 作者：未知作者
• 🏷️ 关键词：Alzheimer
• 📝 描述：RNA sequencing and molecular analyses linked obesity-driven lipid changes to disrupted neuroimmune signaling, revealing a potential metabolic pathway contributing to Alzheimer’s…
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3. 科学家们提高了一种蛋白质的含量，结果发现老年小鼠变得更强壮、更健康。

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Scientists have identified a protein that appears to put the brakes on the chronic inflammation linked to aging. Older mice with boosted levels of the protein were stronger, more energetic, and had healthier bones than untreated mice. Researchers say the findings could eventually lead to therapies that help people stay healthier and more independent later in life.
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4. 突破性药物逆转皮肤衰老并显著加速愈合

• ✍️ 作者：未知作者
• 🏷️ 关键词：aging
• 📝 描述：Scientists have discovered that a topical anti-aging drug called ABT-263 can dramatically improve wound healing in older skin. The treatment works by removing damaged “senescent” cells that accumulate with age and slow the body’s repair process. In aged mice, wounds healed much faster after treatment, while the drug also activated genes tied to collagen production and tissue regeneration.
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• GSE331465 心外膜脂肪驱动心房心肌病中的巨噬细胞反应 [scRNA-Seq]
• GSE331178 一种类凝集素受体激酶和细菌运动性影响组织特异性的玉米-黄单胞菌相互作用
• GSE331129：暴露于香烟烟雾的AOM诱导结直肠癌小鼠结直肠组织的转录组分析
• GSE331109 斑马鱼BDPrB诱导眼损伤的转录组测序数据，2026年5月13日
• GSE319336 FGFRL1 是前列腺癌中 FGFR 和 AR 信号网络的调节因子 [RNA-seq]
• GSE298867 探索DNMT3a在神经元发育中的功能（细胞系RNA测序）
• GSE297617 发现一种针对泛癌中p53高频突变的治疗性抗体
• GSE247331 探索DNMT3a突变对神经元发育的影响（脑组织RNA测序）
• GSE233650 产前富集环境通过激活AHR-Src通路促进胎儿神经元发育
• GSE293941 富马酸诱导的A激酶锚定蛋白12琥珀酰化加剧肾脏炎症和纤维化
• GSE331008 HIV感染者和未感染者脑组织的单核RNA测序。
• GSE328352 工程化双调蛋白通过组织驻留非免疫细胞的双重再生和免疫调节功能促进组织愈合
• GSE306044 父亲早期生活压力和饮食通过精子 DNA 甲基化和杏仁核转录组改变影响雌性后代的行为 [精子甲基化_F0]
• GSE306034 父亲早期生活压力和饮食通过精子 DNA 甲基化和杏仁核转录组改变影响雌性后代的行为 [F0_Male]
• GSE306033 父亲早期生活压力和饮食通过精子 DNA 甲基化和杏仁核转录组改变影响雌性后代的行为 [F1_Female]
• GSE295485 DNA损伤依赖的Orc6与ISWI在S期的结合调节染色质重塑[ATAC-Seq]
• GSE331360：不同处理条件下野生型 (WT) 和 Ch25h-KO 小鼠骨髓来源巨噬细胞的批量 RNA 测序
• GSE331349 复合物 I 驱动谷氨酰胺依赖性 TCA 循环以支持 MYChigh 乳腺癌细胞的存活
• GSE319442 ICAM1高表达的中性粒细胞通过共生黏附和逆向迁移塑造肿瘤演变和转移
• GSE297401 白血病风险因子 ARID5B 协调 HDAC 介导的转录抑制
• GSE297398 白血病风险因子 ARID5B 协调 HDAC 介导的转录抑制 [CUT&Run]
• GSE331446 心外膜脂肪驱动心房心肌病中的巨噬细胞反应
• GSE331245 SMART：三阴性乳腺癌反应轨迹的时空分子图谱
• GSE331154 对注射生理盐水或编码 eGFP 的 mRNA-LNP 的小鼠肝脏进行批量 RNA 测序，剂量为 10 微克，24 小时时间点，静脉注射途径。
• GSE331118 肠毒素性大肠杆菌的鞭毛调控调节先天免疫激活
• GSE331114 颅骨骨髓-淋巴-脑轴介导CD8 T细胞迁移并参与缺血性卒中后损伤 01
• GSE331068 柽柳素诱导A549非小细胞肺癌细胞DNA损伤反应并激活p53信号通路
• GSE327475 基因敲低Emb对小鼠肠神经元发育的影响
• GSE317205 FGFRL1 是前列腺癌中 FGFR 和 AR 信号网络的调节因子
• GSE297662 探索DNMT3a在神经元发育中的功能（WGBS）
• GSE291923 ORCA介导的多梳抑制复合物稳定化维持3D基因组结构并控制复制时间[NS-seq]
• GSE267948 肺结核和肺癌患者外周血单核细胞的基因表达谱
• GSE247332 探索 DNMT3a 突变对神经元发育的影响 (RRBS)
• GSE240630 研究DNMT3a突变对类器官发育的影响[RNA-seq]
• GSE289961：内皮细胞对T细胞疗法的时空单细胞分析