论文精读

巨噬细胞—伤害感受器机械感受中继驱动慢性内脏痛

An autonomous macrophage-nociceptor mechanosensory relay drives chronic visceral pain

有 DOI 和期刊的单篇原创研究，按本库规则保存结构化 paper note

DECODE: Deep learning-based common deconvolution framework for various omics data

DECODE 是一项面向多组学 bulk 数据细胞组成解析的深度学习去卷积框架。论文关注的核心问题是：如何从组织水平的转录组、蛋白组和代谢组数据中，统一、稳健地推断细胞类型和细胞状态丰度。传统去卷积方法多为单一组学设计，难以跨数据类型、平台和队列泛化；DECODE 则试图提供一个可迁移的通用框架，将多组学队列数据扩展到细胞分辨率层面。 中文题名：DECODE：基于深度学习的各种组学数据的通用反卷积框架。 中文摘要：去卷积算法能够从组织水平数据中估计细胞类型丰度，从而支持大规模

单细胞多组学速率深度模型预测 B 细胞中的功能缺失与救援扰动

Deep dynamical models of single-cell multiomic velocities predict loss-of-function and rescue perturbations in B cells

有 DOI 和期刊的单篇原创研究；按本库规则保存结构化 paper note

Deep-Phase：从凝聚体形态解码功能扰动

Cell IF≈50 中科院1区 2026-06-04 (Epub) Donlic A, Comi TJ, Quinodoz SA, Jaberi-Lashkari N, Fernandes KA, Jiang L, Wiesner LW, Lim AI, Brangwynne CP. Cell. 2026;189(15):4562-4580.e10. PMID: 42242225 DOI: 10.1016/j.cell.2026.05.010 生物分子凝聚体（biomole

Deep learning of functional perturbations from condensate morphology

这篇论文提出 Deep-Phase ，用深度学习从显微图像中定量解码生物分子凝聚体形态，并把核仁、核斑和病毒包涵体的形态变化连接到 RNA 转录、加工和核仁亚区组织等功能扰动。 来源层级：文献 / Sources / Papers 主题连接：生物分子凝聚体、核仁、rRNA加工、表型图像分析、深度学习、虚拟细胞 细胞扰动 可提升到 Knowledge/ 的候选概念：凝聚体形态作为功能扰动读出、Deep-Phase、TOP1-rRNA加工-核仁组织、图像表型到分子机制映射 作者想

Hyaluronic acid and tissue mechanics orchestrate mammalian digit tip regeneration

Tissue regeneration is rare in mammals, but the digit tip can regrow after amputation, whereas injuries beyond the nail do not. We found that the ECM and tissue mechanics govern the amputation response. Nonregenerative regions were stiffer and contained dense, organized collagen, whereas regenerative regions were soft and enriched in hyaluronic acid (HA). Depleting HA inhibited regeneration and promoted fibrosis. Stabilization of HA with HAPLN1 after nonregenerative amputations tuned ECM mechanics, reduced scarring, and enhanced bone repair. ECM-targeted strategies could help unlock mammalian regeneration.

文献汇报：透明质酸与组织力学协同调控哺乳动物指端再生

期刊 ：Science Vol 392, Issue 6794 IF ≈ 63.8（中科院 1 区） 发表日期 ：2026-04-09 作者 ：Byron W. H. Mui（剑桥大学 & NIH）等 18 位作者 Zotero ItemID ：1879 Key: ZCMDK2DP DOI ：10.1126/science.ady3136 原文链接 ：https://doi.org/10.1126/science.ady3136 哺乳动物的肢体再生能力极为有限，大多数组织损伤

Chemokine-defined macrophage niches establish spatial organization of tumor immunity

项目 内容 原文题名 Chemokine-defined macrophage niches establish spatial organization of tumor immunity 中文题名 趋化因子定义的巨噬细胞生态位建立肿瘤免疫的空间组织 期刊 Nature Immunology 发表信息 2026-03-23 online；2026 Apr, 27(4):715-724 作者 Soubhik Ghosh, Xin Li, Kavita Rawat, Aishw

CAR-M2免疫治疗通过促进再血管化并诱导促纤维化Cxcr2+内皮细胞凋亡缓解肾纤维化

CAR-M2 immunotherapy resolves renal fibrosis via revascularization and apoptosis of profibrotic Cxcr2+ endothelial cells

Renal fibrosis is a common outcome of chronic kidney disease (CKD), forming a fibrotic niche characterized by fibroblast activation and vascular rarefaction. Currently, there are no effective treatment strategies targeting fibrotic niche. Here, we show that chimeric antigen receptor-modified M2 macrophages (CAR-M2) targeting FAP and secreting interleukin (IL)-4 are delivered via an injectable HAMA-CS hydrogel beneath the renal subcapsule and attenuate renal fibrosis while promoting renal revascularization. The single-cell RNA sequencing reveals the heterogeneity and interaction of stroma and endothelial cells (ECs). A fibrosis-related Cxcr2+ EC subset is identified, and its specific depletion effectively mitigates renal fibrosis. Further results reveal that CAR-M2 can release matrix metalloproteinase 2 (MMP2) in close proximity to activate retinoid X receptor alpha (Rxra) in the Cxcr2+ ECs and further triggers its mitochondrial autophagy, leading to apoptosis. Our research provides innovative strategies and proof of principle for the immunotherapy of organ fibrosis.

The skin microbiota drives cutaneous immune checkpoint inhibitor toxicity in genetically susceptible mice

Immune checkpoint inhibitors (ICIs) show increasing promise for cancer therapy. However, patients can experience adverse events, particularly those with pre-existing autoimmune disease. We determined that the microbiome can drive ICI-induced systemic toxicity in a mouse model of autoimmune susceptibility. Specifically, ICI treatment of specific pathogen-free (SPF) Act1-/- mice, which develop spontaneous autoimmunity due to a deficiency in an immune adaptor, resulted in systemic adverse events that were ameliorated by topical antibiotics. Moreover, germ-free (GF) Act1-/- mice failed to develop ICI toxicity. Transfer of gut or skin microbiota from SPF Act1-/- mice to GF Act1-/- mice showed that only the skin microbiota rendered exGF mice sensitive to ICI toxicity. Notably, therapeutic application of topical antibiotics decoupled ICI-induced toxicity from anti-tumor efficacy in SPF Act1-/- mice. This model provides a paradigm for future translational studies in cancer patients to mitigate adverse effects of ICIs and maximize their efficacy by targeting skin microbes.

文献汇报 | Cell Host & Microbe (2026)

The skin microbiota drives cutaneous immune checkpoint inhibitor toxicity in genetically susceptible mice Salazar V, Espenschied ST, Fernandez AP, Karell PE, Sangwan N, Stappenbeck TS 期刊 ：Cell Host & Microbe 2026 Apr 8;34(4):588-599.e6 PMID

Metabolite-gated vascular contractility switch: OXGR1 activation mechanism enables agonist therapy for rosacea erythema

Xiao et al. identify α-KG as a rosacea-associated metabolite that activates the OXGR1-Gq-MYL9 axis in the vascular smooth muscle cells to boost contractility and suppress pathological vasodilation underlying erythema. Cryo-EM reveals a bipartite-acid pocket of OXGR1 that enables structure-guided development of A-1, a selective agonist that alleviates erythema in rosacea-like models.

OXGR1 激活机制与玫瑰痤疮红斑治疗

Cell IF=45.5 中科院1区 2025-07-11 Xiao WQ, Zhu Y, Tang XJ, Zhu KK, et al. Zotero ItemID: 1872 DOI: 10.1016/j.cell.2026.01.036 玫瑰痤疮（酒渣鼻）是一种慢性炎症性皮肤病，全球患病率约 5.5% ，主要表现为面部中央潮红、持续性红斑、丘疹、脓疱和鼻赘，严重损害患者身心健康。持续性红斑被广泛认为是玫瑰痤疮的主要特征之一。 目前 FDA 批准的红斑治疗药物仅有溴莫尼定

BioAgent Bench - An AI Agent Evaluation Suite for Bioinformatics

核心贡献 ：提出了 BioAgent Bench，一个用于评估 AI Agent 在生物信息学任务中表现的标准测试集和评测框架。 关键发现 ： 前沿闭源模型（Claude Opus 4.5, Gemini 3 Pro, GPT-5.2）可可靠完成端到端生物信息学流程，完成率 90% 开放权重模型表现明显落后，最佳的 GLM-4.7 也仅达 82.5% 鲁棒性测试揭示：即使高层流程构建正确，Agent 在扰动条件下（损坏输入、诱饵文件、提示膨胀）仍会出现失败 生物信息学是 AI

文献汇报 | Zhang et al. 2026 | PAT–KYN–铁蛋白自噬轴介导铁死亡抵抗

Peritumoural adipose tissue promotes ferroptosis resistance by 3-hydroxykynurenine-mediated suppression of ferritinophagy 期刊 ：Nature Cell Biology（NCB） 发表日期 ：2026年3月11日 DOI ：10.1038/s41556-026-01907-x 通讯作者 ：Huai-Qiang Ju（aju-HQ）、Rui-Hua Xu 第

Peritumoural adipose tissue promotes ferroptosis resistance by 3-hydroxykynurenine-mediated suppression of ferritinophagy - Nature Cell Biology

The peritumoural adipose tissue (PAT) is a key contributor to cancer therapy resistance, yet its role in regulating ferroptosis remains unclear. Here we demonstrate that PAT confers ferroptosis resistance to cancer cells by upregulating ferritin (FTH1/FTL) and sequestering intracellular iron. PAT-derived kynurenine (KYN) was identified as the principal mediator. KYN is taken up by cancer cells and metabolized to 3-hydroxykynurenine, which directly binds to nuclear receptor coactivator 4 (NCOA4). This interaction inhibits NCOA4-mediated ferritinophagy, preventing ferritin degradation and limiting the free iron pool required for ferroptosis. In murine models, pharmacological inhibition of the KYN pathway synergized with PD-1 blockade to overcome ferroptosis resistance and suppress tumour progression. These findings reveal a PAT–KYN–ferritinophagy axis that promotes ferroptosis resistance, highlighting the potential of targeting adipose–tumour cross-talk to enhance immunotherapy in PAT-associated tumours. Zhang, Han, Tan, Lu, Ma et al. report that kynurenine derived from peritumoural adipose tissue is hijacked by cancer cells to mediate ferroptosis resistance, a process that could potentially be targeted with immunotherapy to inhibit tumour growth.

GREM1 通过 LEPR 阳性骨骼细胞介导植入周纤维化

GREM1 acts in leptin receptor-expressing skeletal cells to mediate peri-implant fibrosis - Nature Communications

Globally, approximately 1.3 million total joint implants are placed annually, and around 80,000 patients develop aseptic loosening, a leading cause of implant failure driven by peri-implant fibrosis. Here, we show that the BMP-antagonist Gremlin-1 (GREM1), expressed by leptin receptor–expressing skeletal (LEPR+) cells, is a key regulator of this process. GREM1 is highly expressed by LEPR+ cells in peri-implant fibrotic tissue in mice and humans. Conditional deletion of Grem1 in LEPR+ cells attenuate peri-implant fibrosis and enhances peri-implant osteogenesis. Transcriptomic and functional analyses show that loss of Grem1 in LEPR+ cells upregulate the bone morphogenetic protein (BMP) and WNT pathways, increasing in vivo osteogenesis and reducing fibrous tissue formation. As proof-of-concept, intra-articular administration of a neutralizing antibody against GREM1 (anti-GREM1) in mice prevents and reverses peri-implant fibrous tissue while promoting peri-implant bone formation. Inhibition of GREM1 in LEPR+ cells therefore represent a promising strategy to prevent and treat aseptic loosening.

GREM1 通过 LEPR+ 骨骼细胞介导植入周纤维化

Nature Communications IF=16.6 中科院1区 2026-03-23 Vincentius Jeremy Suhardi, Anastasia Oktarina, Yingzhen Niu, et al. DOI: 10.1038/s41467-026-70111-0 GREM1 通过 LEPR 阳性骨骼细胞介导植入周纤维化 全球每年约有 130 万例关节植入手术实施，其中约 8 万名患者会发生无菌性松动；而植入周纤维化是导致植入失败的主要原因之一。本

腱周感觉神经中 YAP1/pSTAT3/NRP1 轴的激活促进肌腱愈合

Activation of the YAP1/pSTAT3/NRP1 axis in peritendinous sensory nerves promotes tendon healing

Chemotactic migration of peritendinous nerves is essential for tendon regeneration, yet the underlying neuroelectrical mechanisms remain unclear. Here, we identify an electrically responsive yes-associated protein 1 (YAP1)/phosphorylated signal transducer and activator of transcription 3 (pSTAT3)/neuropilin-1 (NRP1) signaling axis in sensory neurons. Electrical stimulation enhances YAP1-pSTAT3 interaction, promotes pSTAT3 nuclear translocation and transcriptional activity, and up-regulates NRP1 to support growth of calcitonin gene-related peptide (CGRP)–positive sensory fibers. Guided by these findings, we engineered a bifunctional piezoelectric patch composed of poly(vinylidene difluoride-trifluoroethylene) [P(VDF-TrFE)] and regenerated silk fibroin@poly(3,4-ethylenedioxythiophene):polystyrene sulfonate (RSF@P:P), coupling mechanically induced electrical cues with dynamic lubrication. Under ultrasound activation, the P(VDF-TrFE) layer generates localized electrical signals that facilitate sensory-nerve and vascular ingrowth, while the RSF@P:P layer undergoes piezoelectric-triggered gel-sol transition to form a low-friction interface and reduce adhesion. In rat and Bama minipig models, the patch markedly enhanced tendon regeneration and decreased adhesion scores by ~50%. These findings establish a neuroelectrically guided strategy for enhancing tendon healing.

Reciprocal regulation of fibroblast–macrophage equilibrium governs skin integrity

Fibroblast-macrophage crosstalk is well-established in vitro, and fibroblast-derived colony-stimulating factor 1 (CSF1) supports macrophages in select tissues. However, whether macrophages regulate fibroblasts in vivo remains unknown. Leveraging genetic mouse models, single-cell multi-omics, flow cytometry and imaging, we show that fibroblast depletion or loss of fibroblast-derived growth factors impacts skin macrophage populations in the dermis and hypodermis. Conditional deletion of Csf1 in Dpt+ fibroblasts progressively decreases CD64+ and CD11c+ macrophages, impairing skin wound healing. Reduced macrophage abundance disrupts fibroblast cell cycle regulation, metabolism and immune signaling, and increases fibroblast abundance, affirming a reciprocal relationship. In human systemic sclerosis (scleroderma), elevated fibroblast-derived CSF1 and increased macrophage abundance correlate with disease severity, implicating the CSF1-CSF1R axis in pathology. These findings provide in vivo evidence of macrophage regulation of fibroblasts, revealing a bidirectional interplay that advances understanding of tissue homeostasis and immune regulation in skin.

Lactylome-based investigation of osteoarthritic subchondral bone reveals cell-specific differential expression of histone H4K12 lactylation

译名： 基于乳酰化组的骨关节炎软骨下骨研究揭示组蛋白 H4K12 乳酰化的细胞特异性差异表达：一项实验研究 发表： International Journal of Surgery IF = 10.3（中科院1区） 2026-02-12 DOI： 10.1097/JS9.0000000000004934 通讯作者： Jun Miao（缪俊）, Lin Chen（陈林）等 单位： 上海市第六人民医院 上海交通大学 复旦大学 等 骨关节炎（OA） 是最常见的慢性关节疾病，严重危害

Lactate derived from macrophages drives skin dermal fibroblasts phenotypic remodeling via MCT1-primed histone H3 lysine 23 lactylation in hypertrophic scar - Nature Communications

Hypertrophic scar (HS) is a fibroproliferative disorder characterized by fibroblast hyperactivation and aberrant extracellular matrix deposition. This study identifies macrophage-derived lactate as a key mediator of fibroblast phenotypic remodeling via monocarboxylate transporter 1 (MCT1)-mediated histone H3 lysine 23 lactylation (H3K23la) in HS. Elevated lactate levels and MCT1 expression were observed in HS tissues, with macrophages in stiff mechanical microenvironments identified as the primary lactate source. Lactate influx through MCT1 upregulated H3K23la, thereby promoting transcriptional activation of profibrotic genes HEY2 and COL11A1. Mechanistically, HEY2 activated YAP1/SMAD2 signaling, while COL11A1 stabilized MCT1 to enhance lactate transport, forming a positive loop that amplified fibrosis. Fibroblast-specific Mct1 deletion or pharmacological inhibition of Mct1 in male mice reduced collagen deposition, accelerated wound healing, and attenuated scar formation. Our findings redefine the macrophage-fibroblast crosstalk in HS and establish the MCT1-H3K23la-HEY2/COL11A1 axis, particularly its self-reinforcing loop, as a novel therapeutic target. The study identified macrophage-derived lactate as a driver of hypertrophic scar. Lactate influx via MCT1 triggers histone lactylation in fibroblasts to activate profibrotic genes.

Single-cell transcriptomics and spatial validation reveal dysfunction of keratinocytes and NK cells driving acne development

本文献笔记由 Codex 根据 Zotero 条目、期刊页面和公共数据库核验结果整理。2026-05-11 已通过 Zotero local API 核验条目；PDF 原文来自重复条目 YYVJEWVU 的附件 3U8HNECV ，已同步到本文件夹：Wang 2026 SciRep 角质形成细胞-NK细胞-痤疮.pdf。 这篇文章提出痤疮进展中的 “免疫-屏障双重失衡” 模型：轻度阶段角质形成细胞偏向抗菌和屏障防御，重度阶段出现异常分化和病理性角化；NK 细胞早期参与炎症放大

代谢支持保护放射性黏膜炎中的黏膜免受铁死亡

Metabolic support protects mucosa from ferroptosis in radiation-induced mucositis 代谢支持可保护黏膜免受放射性黏膜炎中的铁死亡 Metabolic support protects mucosa from ferroptosis in radiation-induced mucositis 字段 内容 期刊 Nature Communications 发表时间 2025-12-08 IF（5年I

代谢支持可保护黏膜免受放射性黏膜炎中的铁死亡

Metabolic support protects mucosa from ferroptosis in radiation-induced mucositis

Ionizing radiation is effective in treating cancer but causes significant damage to the mucosa, thereby increasing patient discomfort, delaying therapy, and raising the risk of mortality. The underlying mechanisms of this damage remain poorly understood, and current treatments are largely palliative. In this study, ferroptosis was identified as the primary mode of cell death responsible for the radiation-induced depletion of oral mucosal epithelial cells. Notably, a compensatory phase was also discovered in the early stages following radiation exposure, during which fibroblasts provide crucial metabolic support. Specifically, fibroblasts supply polyamines that are readily absorbed by basal epithelial cells, protecting them from ferroptosis. Supplementation with polyamines was found to effectively prevent mucosal injury. These findings highlight the critical role of fibroblast-mediated metabolic support in protecting the oral mucosa from radiation-induced damage and offer insights into enhancing the body's intrinsic protective mechanisms against radiation-related diseases.

Biomaterial-mediated Cell Atlas: an insight from single-cell and spatial transcriptomics

项目 内容 原文题名 Biomaterial-mediated Cell Atlas: an insight from single-cell and spatial transcriptomics 中文题名 生物材料介导的细胞图谱：来自单细胞和空间转录组学的启示 期刊 Bioactive Materials 发表信息 2025-08-08 online；2025 Dec, 54:1-33 作者 Xiaokun Yang, Mingshu Huang, Huan Chen,

A biomimetic senotherapy replenishing MAT2A promotes wound regeneration in preclinical models

中文译名 ：仿生衰老疗法补充 MAT2A 促进临床前模型中的伤口再生 发表期刊 ：Nature Communications (2025) 16:10580 DOI ：10.1038/s41467-025-65659-2 第一作者 ：Lv Dongming, Ren Lei, Zhao Zirui, Rong Yanchao（并列第一作者） 通讯作者 ：Deng Wuguo, Tang Qing, Tang Bing 单位 ：中山大学附属第一医院整形外科、中山大学肿瘤防治中心

T-cell immunoglobulin and mucin domain-containing protein 3-mediated immunomodulation in myeloid cells and keratinocytes in the development of severe acne

本文献笔记由 Codex 根据 Zotero 条目、期刊页面和公共数据库核验结果整理。2026-05-11 已通过 Zotero local API 核验条目；PDF 原文来自重复条目 MMW5YS9F 的附件 MM6VWFLP ，已同步到本文件夹：Chen 2025 MolBiomed TIM3-重度痤疮.pdf。 这篇文章把 TIM3 从传统的 T 细胞耗竭/免疫检查点语境，转移到重度痤疮的 髓系细胞-角质形成细胞免疫调控轴 中：作者认为 TIM3 参与限制痤疮炎症，尤其

人类皮肤成纤维细胞的单细胞与空间基因组学图谱:跨组织共享的疾病相关成纤维细胞亚型

A single-cell and spatial genomics atlas of human skin fibroblasts reveals shared disease-related fibroblast subtypes across tissues

Fibroblasts sculpt the architecture and cellular microenvironments of various tissues. Here we constructed a spatially resolved atlas of human skin fibroblasts from healthy skin and 23 skin diseases, with comparison to 14 cross-tissue diseases. We define six major skin fibroblast subtypes in health and three that are disease-specific. We characterize two fibroblast subtypes further as they are conserved across tissues and are immune-related. The first, F3: fibroblastic reticular cell-like fibroblast (CCL19+CD74+HLA-DRA+), is a fibroblastic reticular cell-like subtype that is predicted to maintain the superficial perivascular immune niche. The second, F6: inflammatory myofibroblasts (IL11+MMP1+CXCL8+IL7R+), characterizes early human skin wounds, inflammatory diseases with scarring risk and cancer. F6: inflammatory myofibroblasts were predicted to recruit neutrophils, monocytes and B cells across multiple human tissues. Our study provides a harmonized nomenclature for skin fibroblasts in health and disease, contextualized with cross-tissue findings and clinical skin disease profiles.

骨桥蛋白减轻硅胶植入物的异物反应

Osteopontin attenuates the foreign-body response to silicone implants

Silicone implants are widely used in plastic and reconstructive surgery, but their efficacy is limited by the foreign-body response (FBR), which causes capsular contracture, implant failure, and secondary surgeries. Acellular dermal matrices (ADMs) reduce the FBR clinically, but the molecular mechanism is unclear. Here we show that osteopontin (SPP1) secreted by monocyte/macrophage clusters adjacent to the ADM is both necessary and sufficient to attenuate the FBR to silicone implants, and that SPP1 acts via CD44 receptor signalling and upregulation of matrix metalloproteinase 9. Sustained local delivery of SPP1 via injectable, self-healing polymer-nanoparticle hydrogels phenocopies the protective effect of ADMs in both immunocompetent and SPP1-knockout mice, suggesting a potential strategy to mitigate the FBR without the need for ADMs.

EGFR-STAT1 pathway drives fibrosis initiation in fibroinflammatory skin diseases

Odell et al., 2025, Nature Medicine The EGFR-STAT1 axis drives fibrosis across fibroinflammatory skin diseases including systemic sclerosis (SSc), hidradenitis suppurativa (HS), and lupus. Epidermal keratinocytes in these diseases upregulat

通过功能性抑制瘦素受体阳性骨骼细胞预防和治疗植入周纤维化

Prevention and treatment of peri-implant fibrosis by functionally inhibiting skeletal cells expressing the leptin receptor - Nature Biomedical Engineering

The cellular and molecular mediators of peri-implant fibrosis—a most common reason for implant failure and for surgical revision after the replacement of a prosthetic joint—remain unclear. Here we show that peri-implant fibrotic tissue in mice and humans is largely composed of a specific population of skeletal cells expressing the leptin receptor (LEPR) and that these cells are necessary and sufficient to generate and maintain peri-implant fibrotic tissue. In a mouse model of tibial implantation and osseointegration that mimics partial knee arthroplasty, genetic ablation of LEPR+ cells prevented peri-implant fibrosis and the implantation of LEPR+ cells from peri-implant fibrotic tissue was sufficient to induce fibrosis in secondary hosts. Conditional deletion of the adhesion G-protein-coupled receptor F5 (ADGRF5) in LEPR+ cells attenuated peri-implant fibrosis while augmenting peri-implant bone formation, and ADGRF5 inhibition by the intra-articular or systemic administration of neutralizing anti-ADGRF5 in the mice prevented and reversed peri-implant fibrosis. Pharmaceutical agents that inhibit the ADGRF5 pathway in LEPR+ cells may be used to prevent and treat peri-implant fibrosis.

功能性抑制 LEPR+ 骨骼细胞防治植入周纤维化

Nature Biomedical Engineering IF=24.6 中科院1区 2024-07-31 Vincentius Jeremy Suhardi, Anastasia Oktarina, Mohammed Hammad, et al. DOI: 10.1038/s41551-024-01238-y 通过功能性抑制瘦素受体阳性骨骼细胞预防和治疗植入周纤维化 植入周纤维化是人工关节置换后植入失败及翻修手术最常见的原因之一，但其细胞与分子介质尚不清楚。本研究表明，小

基于图关联统一嵌入的单细胞多组学整合与调控推断

基于图关联统一嵌入的单细胞多组学数据整合与调控推断 Multi-omics single-cell data integration and regulatory inference with graph-linked embedding Nature Biotechnology IF=41.7 中科院1区 2022-05-02 Zhi-Jie Cao, Ge Gao DOI: 10.1038/s41587-022-01284-4 尽管单细胞中同步测量多种组学模态的实验方法已

基于图关联统一嵌入的单细胞多组学数据整合与调控推断

Multi-omics single-cell data integration and regulatory inference with graph-linked embedding

Despite the emergence of experimental methods for simultaneous measurement of multiple omics modalities in single cells, most single-cell datasets include only one modality. A major obstacle in integrating omics data from multiple modalities is that different omics layers typically have distinct feature spaces. Here, we propose a computational framework called GLUE (graph-linked unified embedding), which bridges the gap by modeling regulatory interactions across omics layers explicitly. Systematic benchmarking demonstrated that GLUE is more accurate, robust and scalable than state-of-the-art tools for heterogeneous single-cell multi-omics data. We applied GLUE to various challenging tasks, including triple-omics integration, integrative regulatory inference and multi-omics human cell atlas construction over millions of cells, where GLUE was able to correct previous annotations. GLUE features a modular design that can be flexibly extended and enhanced for new analysis tasks. The full package is available online at https://github.com/gao-lab/GLUE.

Impact of gut microbiome on skin health: gut-skin axis observed through the lenses of therapeutics and skin diseases

Mahmud et al. 系统综述了肠道微生物组与皮肤健康之间的相互作用（肠-皮肤轴），涵盖健康皮肤和肠道的微生物生态、饮食因素（母乳/配方奶、高/低脂饮食、蛋白质饮食、膳食纤维）、药物（抗生素、益生元、益生菌、新型生物制剂）对肠道微生物组及皮肤的影响，及其与银屑病、特应性皮炎、寻常痤疮、酒渣鼻、斑秃、化脓性汗腺炎等皮肤疾病的关联。