Cells细胞
Cells(英文缩写 CELLS-BASEL),ISSN 2073-4409,eISSN 2073-4409,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
Cells 最新收录文献
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1. Blood-Mediated Gut-Brain Axis in Parkinson's Disease: Focus on α-Synuclein Transport and Microbiota Dysbiosis-Induced Inflammation.
PMID:日期:2026-09-21Parkinson's disease (PD) is a progressive neurodegenerative disorder characterized by the loss of dopaminergic neurons and the deposition of Lewy bodies (LBs). The gut-brain axis has emerged as a potential route for the bidirectional dissemination of PD pathology, in which the enteric and central nervous systems may contribute to the spread of misfolded α-synuclein (α-Syn) and associated neuroinflammatory responses. However, neural pathways alone may not fully account for the widespread distribution of PD pathology across the brain and gut. As another major conduit connecting the gut and the brain, the peripheral circulation may provide an additional route for PD-related pathological processes. Nevertheless, how blood circulation contributes to the development and dissemination of pathology along the gut-brain axis remains underexplored. Accordingly, this narrative review examines peripheral blood as a potential additional route for pathological communication along the gut-brain axis, focusing on two potential mechanisms involving the transport of pathological α-Syn aggregates between the gut and the brain and the circulation of inflammatory signals associated with gut microbiota dysbiosis. Furthermore, to highlight the translational relevance of the gut-blood-brain axis, we briefly summarize recent advances in related blood-derived biomarkers and therapeutic strategies targeting these pathways.
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2. Systemic Inflammatory Response During Coronary Artery Bypass Grafting with Cardiopulmonary Bypass: Cellular and Molecular Mechanisms.
PMID:日期:2026-09-21Coronary artery bypass grafting (CABG) utilizing cardiopulmonary bypass (CPB) remains a cornerstone of treatment for advanced multivessel coronary artery disease. During the ischemic period, myocardial cells become injured and increasingly depend on anaerobic metabolism. After reperfusion, exposure of blood components to artificial surfaces, combined with ischemia-reperfusion injury, surgical trauma, and gut translocation of endotoxins, triggers a complex systemic inflammatory response syndrome (SIRS). This inflammatory cascade involves a tightly regulated network of humoral cascades (complement, contact, coagulation, and fibrinolytic systems) and cellular effectors (neutrophils, monocytes, endothelial cells, and platelets). Molecular signaling pathways, notably Toll-like receptor 4 (TLR4) activation, nuclear factor kappa B (NF-κB) nuclear translocation, mitogen-activated protein kinase (MAPK) phosphorylation, and NLRP3 inflammasome assembly, drive a cytokine storm characterized by massive releases of interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-8 (IL-8). These molecular events lead to endothelial barrier disruption, vasoplegic shock, acute lung injury, myocardial dysfunction, and acute kidney injury. This comprehensive narrative review provides a detailed synthesis of the cellular and molecular mechanisms underlying CPB-induced SIRS, highlights recent advances in neutrophil extracellular trap (NET) dynamics and microvascular injury, and evaluates contemporary pharmacological and bioengineering therapeutic strategies designed to mitigate postoperative organ dysfunction.
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3. Targeting NCAM1/FGFR1 Signaling to Alleviate Sleep Disturbance-Induced Neuroinflammation in the Hypothalamus.
PMID:日期:2026-09-21Sleep disturbance is a prevalent public health concern associated with cognitive deficits and emotional dysregulation, yet the mechanisms underlying SD-induced hypothalamic dysfunction remain incompletely understood. Here, we found that two weeks of SD induced marked hypothalamic neuroinflammation, accompanied by increased expression of the pro-inflammatory cytokines , , and , as well as the chemokine , together with reduced neuronal markers, including decreased Nissl-body and NeuN cells. Single-nucleus RNA sequencing (snRNA-seq) suggested that inhibitory neurons exhibited prominent transcriptional responses to SD, including enrichment of inflammatory pathways such as TNF and IL-17 signaling and transcriptional programs associated with neuronal dysfunction. Furthermore, SD was also associated with microglial activation and a phenotypic shift toward a disease-associated state, exhibiting enhanced antigen-presenting and pro-inflammatory capacity. Notably, intercellular communication analysis identified the neural cell adhesion molecule 1 (NCAM1)/fibroblast growth factor receptor 1 (FGFR1) signaling axis as a key mediator of crosstalk between microglia and other cell types. In BV2 cells, recombinant NCAM1 attenuated lipopolysaccharide-induced inflammatory responses in an -dependent manner. Consistently, PVN-targeted knockdown in vivo exacerbated SD-associated microglial activation, neuroinflammation, and neuronal injury. Collectively, our findings elucidate a critical protective role for the NCAM1/FGFR1 axis in mitigating SD-induced hypothalamic neuroinflammation and neuronal injury. This highlights this pathway as a candidate mechanism for further therapeutic investigation in sleep-related neurological dysfunction.
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4. Bladder Sensory Neurons as Regulators of Neuro-Immune-Urothelial Interactions: From Molecular Mechanisms to Targeted Therapy for Neurogenic Bladder and Interstitial Cystitis/Bladder Pain Syndrome.
PMID:日期:2026-09-21Bladder sensory neurons are essential components of lower urinary tract sensory encoding and micturition reflex control. They detect bladder filling, stretch, inflammatory mediators, and pathogen-associated stimuli, and they communicate with urothelial cells, immune cells, and stromal cells through neuropeptides such as calcitonin gene-related peptide (CGRP), substance P (SP), and vasoactive intestinal peptide (VIP). Under physiological conditions, this neuro-immune-urothelial axis contributes to bladder homeostasis. Under pathological conditions, including neural injury, infection, inflammation, or epithelial barrier disruption, TRP channels, purinergic signaling, neurotrophic factors, chemokines, and voltage-gated ion channels can induce peripheral sensitization, increased excitability of dorsal root ganglion (DRG) neurons, spinal plasticity, and central sensitization, thereby contributing to urinary frequency, urgency, bladder pain, and detrusor overactivity in neurogenic bladder and interstitial cystitis/bladder pain syndrome (IC/BPS). This review summarizes the anatomical and functional organization of bladder sensory afferents, sensory neuron-associated molecular signaling, neuro-immune-urothelial interactions, disease-specific mechanisms, and targeted therapeutic strategies. We also discuss the translational potential and limitations of interventions targeting TRPV1/TRPV4/TRPA1, P2X3, CGRP, SP/neurokinin receptors, NGF, ion channels, botulinum toxin, and neuromodulation. These mechanisms provide a framework for understanding neurogenic mechanisms in bladder disorders and for developing targeted interventions.
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5. Lipidomic Evidence for Cannabidiol-Induced Remodeling of Cellular Lipid Composition in SH-SY5Y Cells.
PMID:日期:2026-09-21Cannabidiol (CBD) is increasingly discussed in relation to neurodegenerative disorders, including Alzheimer's disease (AD), yet its effects on cellular lipid profiles remain poorly understood. Using targeted lipidomics, we investigated whether CBD alters the lipidome of SH-SY5Y wildtype (wt) cells and whether the principal phosphatidylcholine response is also observed in cells expressing amyloid precursor protein with the Swedish mutation (APPswe). CBD induced a broad, class-specific lipid response. Total diacyl and ether-linked phosphatidylcholines increased. Within these classes, many species with lower degrees of unsaturation increased, whereas several highly polyunsaturated ether-linked phosphatidylcholines declined. Lysophosphatidylcholines were broadly reduced, total sphingomyelin abundance declined, free carnitine decreased, and most measured acylcarnitine species also declined. Together, in wt cells, these changes are consistent with a relative shift toward a less polyunsaturated lipid profile. CBD-associated changes in both phosphatidylcholine classes were also observed in stably APPswe-expressing SH-SY5Y cells. Because the affected lipid classes have been implicated in AD-related lipid dysregulation, these findings link CBD exposure to an AD-relevant lipid context and provide a rationale for investigating the functional consequences of this response in more complex neurodegeneration-relevant models.
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6. The p53-Associated Regulation of ATF4 mRNA Expression Involves p21 and p130 in a Stress-Dependent Manner.
PMID:日期:2026-09-20p53-dependent signaling and the integrated stress response (ISR) are major stress response programs that coordinate cellular metabolism and cell fate decisions. While p53 activation often promotes cell cycle arrest and cell death, the ISR can support either adaptive survival or cell death depending on the cellular context. Although increasing evidence indicates the crosstalk between these pathways, the underlying mechanisms remain incompletely understood. Here, we show that p53 activation is associated with reduced ATF4 mRNA expression under basal conditions and during selected metabolic stresses, including mitochondrial dysfunction. Knockdown experiments have demonstrated that p21 and p130 contribute to this response in a stress-dependent manner. Our findings identify a context-dependent link between p53 signaling and ATF4 mRNA regulation and suggest that p53, p21, and p130 may influence the ATF4-dependent branch of the ISR during cellular stress.
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7. Bone Aging and Glycative Stress: Convergent and Divergent Mechanisms Driving Skeletal Deterioration.
7. 骨衰老与糖化应激：驱动骨骼退化的趋同与趋异机制PMID:日期:2026-09-20Aging and glycative stress are major, interrelated drivers of skeletal fragility, yet the extent to which they act through shared versus distinct biological pathways remains poorly defined, limiting integrated therapeutic strategies. This review compares the convergent and divergent mechanisms by which aging and glycative stress affect osteocytes, osteoblasts, and osteoclasts, extracellular matrix properties, and bone mechanotransduction. Both conditions converge on oxidative stress, mitochondrial dysfunction, chronic low-grade inflammation, cellular senescence, impaired autophagy, NLRP3 inflammasome activation, and ferroptosis, ultimately reducing osteocyte viability and disrupting RANKL/OPG-mediated remodeling. They diverge in their primary drivers: Aging is characterized by hormonal decline, stem-cell exhaustion, and progressive loss of bone mass and microarchitecture, whereas glycative stress acts through AGE-RAGE signaling and collagen cross-linking, compromising bone quality and mechanosensitivity while often preserving bone mineral density, explaining the disproportionate fracture risk seen in diabetes. Since current anabolic and anti-resorptive therapies do not specifically target AGE-related pathways, combined strategies incorporating senolytic, antiglycative, and mechanoprotective approaches-alongside lifestyle interventions-may be needed to more effectively reduce fracture risk in aged and diabetic populations.
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8. ERBB4 and Neurodegeneration: Association Between Hypothalamic-Pituitary-Adrenal (HPA) Axis: Associated Neurodegenerative Pathogenesis.
PMID:日期:2026-09-20The hypothalamic-pituitary-adrenal (HPA) axis is the central neuroendocrine system that controls physiological stress responses and maintains homeostasis through the coordinated interactions among the hypothalamus, pituitary gland, and adrenal cortex. Dysregulation of the HPA axis is associated with stress-related psychiatric conditions and neurodegenerative diseases, including Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis. Chronic stress creates a detrimental environment in the brain, inducing structural changes and accelerating brain aging and the loss of neurons. Receptor tyrosine-protein kinase ERBB4 (ERBB4), a member of the epidermal growth factor receptor (EGFR) family, is activated primarily by neuregulin ligands and plays an essential role in neuronal development, synaptic plasticity, and cell survival. Emerging evidence suggests that ERBB4 signaling influences neuroendocrine regulation and stress responsivity. While further studies are needed to provide direct mechanistic evidence linking ERBB4-mediated HPA axis dysregulation to neurodegenerative cell death, this manuscript critically evaluated the preclinical models and proposes a possible feed-forward framework wherein ERBB4 served as a permissive homeostatic modulator at the intersection of stress endocrinology and neuroinflammation. Furthermore, the impact of ERBB4 dysregulation and its mutations on neurodegenerative diseases has been presented, focusing on potential mechanisms of oxidative stress, synaptic dysfunction, and neuronal apoptosis. Taken together, ERBB4 represents an important molecular interface between stress signaling and neurodegenerative pathology. Understanding the regulation of ERBB4 in the HPA axis has provided new insights into the mechanisms underlying neurodegenerative diseases and could identify novel therapeutic targets for stress-associated neurological disorders.
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9. Explicit Mechanistic Operators in Predictive Virtual Cells: Evidence, Failure Modes, and a Minimum Falsification Framework for Single-Cell Perturbation Prediction.
PMID:日期:2026-09-20The term virtual cell now covers objects ranging from curated biochemical simulators to atlas-trained neural representations, yet the decisive empirical question is narrower: whether a model built to obey known biochemical rules predicts the effects of new drugs or genetic changes better than an otherwise identical model that lacks them. Formally, this Perspective asks whether a biologically specified mechanistic operator improves out-of-distribution prediction of single-cell perturbation responses beyond strong simple, relational, transport-based, and learned-dynamical comparators. Recent benchmarks show that rankings depend on partition, statistical unit, effect-size distribution, gene set, and metric, and that several deep and foundation-model approaches fail to exceed no-change, mean-effect, additive, or linear controls. Set-based, knowledge-graph, transport, and learned state-equation models can improve defined tasks. No identified study isolates the incremental value of a biologically specified operator against late fusion, a capacity-matched static model, a capacity-matched learned-dynamical operator, and topology-rewired controls under one locked evaluation. Six source categories are distinguished, with the operator category divided into biologically specified and learned-dynamical subclasses. A minimum falsification framework is specified for the unfolded protein response with a declared capacity ledger, endpoint times chosen by a prespecified Stage 1 rule, and a locked comparator set. The framework is prospective: no new data, model implementation, or performance result is reported, and every threshold is a design choice awaiting empirical test.
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10. Genomic Imprinting in Animals: Evolutionary Conservation with Adaptive Flexibility.
PMID:日期:2026-09-20Imprinting is an epigenetic mechanism found in many diploid organisms that enables discrimination between genetic material inherited from one or the other parent. It has been predominantly studied in mammals, where, in the adult, it affects the expression of a limited set of genes (in most higher mammals) or leads to paternal X chromosome inactivation in marsupials. DNA CpG methylation and heterochromatic epigenetic marks play a crucial role in these processes. Imprinting also exists in other organisms, where it can cause unusual parent-of-origin-dependent effects. Two classical examples are whole paternal genome inactivation in mealybug males and selective paternal X chromosome elimination in fungus gnats. Although these manifestations of imprinting are quite exotic, they share features in common with those observed in mammals, implying that, despite the differences, the core mechanism, the H3K9me3:HP1:H4K20me3 pathway, is evolutionarily conserved across animal phyla. Here, we discuss recent advances that provide further evidence supporting this concept.