CELL细胞
CELL(英文缩写 CELL),ISSN 0092-8674,eISSN 1097-4172,中文译名:细胞 是一本学术期刊。本页汇总该期刊的最新影响因子、分区信息以及最新收录于 PubMed 的文献,帮助您快速了解期刊全貌。
发文量统计区间：2025-09-27 至 2026-09-27，按本站收录文献的发表日期统计。
期刊介绍
历年影响因子趋势
| JCR 数据年份 | 影响因子 | JCR 分区 |
|---|---|---|
| 2021 | 66.850 | Q1 |
| 2022 | 64.500 | Q1 |
| 2023 | 45.500 | Q1 |
| 2024 | 42.500 | Q1 |
| 2025 | 45.100 | Q1 |
CELL 最新收录文献
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1. Resident tissue macrophages transfer selenium transporter protein to protect pancreatic cancer from ferroptosis.
PMID:日期:2026-09-24Pancreatic ductal adenocarcinoma (PDAC), an aggressive cancer with a poor prognosis, contains resident tissue macrophages (RTMs) present before tumor onset and monocyte-derived macrophages recruited during tumor development, but their distinct roles in supporting tumor progression remain unclear. Combining single-cell profiling, spatial analysis, lineage tracing, RTM depletion, and selenium tracing, we found that RTMs preferentially localize at the tumor border, where they promote epithelial-mesenchymal transition (EMT), tumor growth, and metastasis. Mechanistically, RTMs transfer the selenium transporter Selenop to EMT tumor cells through LRP8-dependent uptake, increasing tumor-cell selenium availability, limiting lipid peroxidation, and shielding EMT tumor cells from ferroptosis. RTM-specific Selenop deletion or tumor-cell Lrp8 disruption reduced EMT and tumor progression, whereas ferroptosis inhibition reversed the effect of RTM depletion. Human PDAC showed border-enriched SEPP1 RTMs near EMT tumor cells, suggesting a conserved macrophage-derived selenium niche that supports invasive tumor states and highlighting the potential for targeting RTMs or their secretory factors in PDAC.
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2. A pericyte-to-myofibroblast transition links APOE4 to cerebrovascular degeneration.
PMID:日期:2026-09-24Cerebrovascular disease is a major but poorly understood feature of Alzheimer's disease (AD). The strongest genetic AD risk factor, apolipoprotein E4 (APOE4), is associated with cerebrovascular degeneration, including vascular amyloid deposition and fibrosis. To uncover how APOE4 promotes cerebrovascular pathology, we assembled a single-cell transcriptomic atlas of human brain vasculature. In APOE4 carriers, pericyte abundance was significantly reduced and accompanied by the emergence of a myofibroblast-like cell population co-expressing contraction and extracellular matrix genes. Immunostaining confirmed non-vascular myofibroblasts in APOE4 human and mouse brains. We show that APOE4 pericytes transition into myofibroblasts that secrete fibronectin, which promotes vascular amyloid accumulation. Computational and experimental analyses identified elevated transforming growth factor β (TGF-β) signaling as the driver of this pericyte-to-myofibroblast transition. Inhibition of TGF-β restored pericyte coverage and reduced vascular fibrosis and amyloid to APOE3 levels, revealing a targetable mechanism linking APOE4 to cerebrovascular pathology in AD.
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3. Shifts in embryonic oxygen levels cue heterochrony in limb initiation.
PMID:日期:2026-09-24Heterochrony, or the alteration of developmental timing, is an important mechanism of evolutionary change. Avian species display synchronized growth of the forelimbs and hindlimbs, while mammalian species show delayed hindlimb development. We find that mammalian limb heterochrony is evident from the start of limb bud formation and is associated with heterochronic expression of T-box transcription factors. This heterochronic shift is not due to changes in cis-regulatory sequences controlling T-box gene expression but, unexpectedly, is dependent upon the differential oxygen levels to which avian and mammalian embryos are exposed prior to limb initiation. This is mediated, at least partially, by cRel, a transcription factor in the nuclear factor κB (NF-κB) family, and by the oxygen-sensing transcription factor hypoxia-inducible factor alpha (Hif1a). Together, these results provide a mechanistic understanding of an important example of developmental heterochrony and exemplify how the maternal environment can regulate timing during embryonic development.
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4. CD4 T cells convert transient responses to KRAS inhibition to durable remissions in pancreatic cancer.
PMID:日期:2026-09-23Pancreatic ductal adenocarcinoma (PDAC) is refractory to most therapies, including immunotherapies, for which reinvigoration of CD8 T cells through immune checkpoint blockade is insufficient to induce long-term, durable remissions. Direct KRAS inhibitors (KRASi) have shown clinical promise, although acquired resistance is common. We modeled KRASi response and relapse in mice and demonstrated that, unlike chemotherapy or combinations with checkpoint blockade, an interleukin (IL)-21 cytokine mimic (21h10) induced long-term, durable remissions. Its efficacy depends on T helper 1 (Th1)-polarized CD4 T cells, but not on CD8 T cells or tumor cell expression of major histocompatibility complex class I (MHC class I). Specifically, CD4 T cells primed by type 2 conventional dendritic cells (cDC2s) produce interferon γ (IFN-γ), which promotes macrophage-mediated phagocytosis of tumor cells. Ex vivo treatment of human PDAC specimens with 21h10 induces IFN-γ production by infiltrating T cells. Thus, IL-21-elicited CD4 T cells exert antitumor activity in mice and potentially in humans, converting transient responses to KRAS inhibition into durable remissions.
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5. Projection-defined modules reveal mouse motor cortex architecture.
PMID:日期:2026-09-23The motor cortex (MO) coordinates movement through its complex connectivity. However, despite evidence for functionally and anatomically distinct areas, organizing principles of MO lack consensus. Here, we show that the subcortical projections of mouse MO define 16 different modules. Subcortical output divergence aligns with variation in modular corticocortical connectivity and cell-type composition, delineating two spatial MO axes. Along one axis, primary MO couples reciprocally to somatosensory cortex and secondary MO to frontal areas, with differential excitatory neuron compositions specifying the two regions. Along the orthogonal axis, somatosensory cortex inputs stratify modules, together with non-sensorimotor cortical wiring and aligned cell-type signatures. The cortical two-axis logic extends to subcortical targets, with the striatum, thalamus, and brainstem following distinct convergence-divergence rules, differentially integrating cortical inputs. Together, this work reveals a logic by which the anatomical architecture of the mouse MO integrates into brainwide and specific neuronal networks.
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6. Direct cell-to-cell transmission of retrotransposons.
PMID:日期:2026-09-23Transposable elements are abundant in host genomes but are generally considered to be confined to the cell in which they are expressed, with the notable exception of endogenous retroviruses. Here, we identify a group of long terminal repeat (LTR) retrotransposons that infect the germline from somatic cells within the Drosophila ovary, despite lacking the fusogenic Envelope protein typically required for retroviral entry. Instead, these elements encode a short transmembrane protein, sORF2, which bears structural features reminiscent of viral cell-cell fusogens. Through genetics, imaging, and electron microscopy, we show that sORF2 localizes to invasive somatic protrusions that contain retroviral capsids and establish physical contact with the oocyte membrane. In the absence of sORF2, protrusion formation and soma-to-germline transmission of capsids are abolished. Remarkably, sORF2-like proteins are widespread among insect retrotransposons and also occur in piscine nackednaviruses and avian picornaviruses. These findings reveal a noncanonical, Envelope-independent transmission mechanism shared by retrotransposons and non-enveloped viruses.
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7. Microbial signaling coordinates group oviposition and predator defense in migratory locusts.
PMID:日期:2026-09-23Reproductive synchronization is suggested to enhance fitness in many insects, yet the mechanisms enabling such coordination remain unknown. In Locusta migratoria, we identify a microbiota-derived volatile, 2,4,6-trimethylpyridine (2,4,6-TMP) that coordinates communal oviposition in gregarious females while simultaneously deterring egg predators. Eggs laid by gregarious females emit 2,4,6-TMP, which attracts conspecifics by activating the olfactory receptors LmOR34 and LmOR36; disruption of either receptor abolishes attraction and alters oviposition behavior. 2,4,6-TMP is synthesized by the egg-associated bacterium Enterobacter roggenkampii through a lysine degradation pathway. Deletion of lysine decarboxylase abolishes 2,4,6-TMP production and associated behavioral responses. Beyond facilitating reproduction, 2,4,6-TMP repels soil-dwelling predators, including ants, beetles, and potworms. In the ant Solenopsis invicta, avoidance is mediated by the olfactory receptor SinOR43a-1; RNA interference (RNAi) knockdown of this receptor abolishes repellence. Semi-field assays confirm the ecological relevance of 2,4,6-TMP. These findings reveal an egg-associated bacterial signaling mechanism that couples reproductive coordination with predator defense in L. migratoria.
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8. Switching of transcriptional control from interferon regulatory factor 2 to interferon regulatory factor 1 drives innate immune cell activation.
PMID:日期:2026-09-22Interferon regulatory factor 2 (IRF2) is a transcription factor that prevents skin inflammation in mice and humans but, paradoxically, promotes pyroptosis by upregulating gasdermin D. How IRF2 activates some proinflammatory genes but suppresses inflammation is unclear. We show that skin inflammation in Irf2-deficient mice is driven by IRF1 activation of interferon-stimulated genes (ISGs). Chromatin profiling reveals that IRF1 and IRF2 occupy the same ISG regulatory sites, but as a weaker transcriptional activator, IRF2 limits ISG transcription by IRF1. Toll-like receptor (TLR) signaling favors IRF1-driven transcription by inducing Irf1. In addition, IRF1 recruits the ubiquitin ligase SPOP to ISG sites, resulting in proteasomal degradation of IRF2. This shift from IRF2 to IRF1 occupancy enhances ISG transcription. Collectively, these findings define a hierarchical transcriptional circuit in which IRF2 limits IRF1 activity under homeostatic conditions but is displaced during an immune response, allowing IRF1-dependent gene programs central to innate immunity and autoinflammation.
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9. A geothermal amoeba sets a new upper temperature limit for eukaryotes.
PMID:日期:2026-09-22The study of temperature limits has transformed our understanding of life's boundaries but has focused on bacteria and archaea. For decades after their discovery, no eukaryote was shown to replicate above 60°C. We isolated a geothermal amoeba, Incendiamoeba cascadensis, that divides at 63°C and is motile up to 64°C. We identified an enrichment of genes related to proteostasis and environmental sensing relative to mesophilic amoebae. Comparative RNA sequencing of I. cascadensis revealed upregulation of pathways related to proteostasis, DNA repair, and membrane trafficking at high temperatures. Predicted proteins of I. cascadensis have distinct biophysical properties, including enrichment of positively charged surface residues similar to bacterial and archaeal hyperthermophiles, which suggests a convergent mechanism for protein stability under temperature stress. Together, our findings expand our understanding of where and how life can persist.
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10. Oligodendrocytes in central nervous system health and disease.
PMID:日期:2026-09-18Oligodendrocytes are a specialized class of glial cells responsible for myelination, which sustains central nervous system (CNS) function. Though long considered a passive and static cell, the oligodendrocyte is now recognized to actively support axonal energy demands through metabolic provision, modify neural signaling in response to environmental stimuli through adaptive myelination, and repair or regenerate myelin following injury. However, oligodendrocytes become dysfunctional in aging and disease. Emerging research has uncovered that oligodendrocytes can even contribute to CNS pathology themselves, making them novel therapeutic targets for neurological disease. In this review, we highlight key advancements to our understanding of oligodendrocytes in development, homeostasis, aging, and disease and how their heterogeneity influences their roles in these contexts. We highlight outstanding questions that require further study to progress our understanding of oligodendrocytes.