iMeta
iMeta(英文缩写 IMETA),ISSN 2770-5986,eISSN 2770-596X 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：2025-11-01 至 2026-10-31，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 |
|---|---|---|
| 2023 | 23.700 | Q1 |
| 2024 | 33.200 | Q1 |
| 2025 | 44.400 | Q1 |
iMeta 最新收录文献
-
1. Deciphering transcriptome complexity via long-read sequencing.
1. 通过长读长测序破译转录组复杂性PMID:日期:2026-10-04Transcriptomics is moving beyond gene-level quantification toward isoform-resolved interrogation of alternative splicing, transcript structural variation, and repeat-derived transcription. Yet short-read sequencing remains intrinsically limited in accurately reconstructing full-length transcripts and resolving complex repetitive regions, including transposable elements. Recent advances in long-read sequencing, exemplified by Pacific Biosciences (PacBio) and Oxford Nanopore Technologies (ONT), offer a transformative opportunity to directly observe complete RNA molecules and thereby overcome these bottlenecks. However, practical adoption is hindered by demanding library construction and the need to process noisy, fast-evolving long-read data, and the field still lacks a unified resource that guides researchers through the entire experimental and analytical workflow. This review fills that gap by providing a concise, end-to-end, and implementation-oriented roadmap for long-read transcriptomics. We distill the key decisions from platform and library strategy selection to core computational processing and downstream interpretation, and we summarize emerging frontiers and best-practice recommendations. By offering a reusable framework and practical checklists, this guide empowers a broader community to exploit long reads for standardized, reproducible, isoform-level discovery at unprecedented resolution.
-
2. Dissecting the angiogenic mechanism of pachychoroid polypoidal choroidal vasculopathy.
2. 剖析厚脉络膜息肉状脉络膜血管病变的血管生成机制PMID:日期:2026-09-30Polypoidal choroidal vasculopathy (PCV) is a distinct variant of neovascular age-related macular degeneration (AMD) and a major cause of vision loss in older adults, yet its pathogenesis remains poorly understood. Pachychoroid PCV is a subtype characterized by poor treatment response, minimal typical AMD features, and dilated choroidal vessels. Using a multicenter PCV cohort, we conducted plasma multi-omics analyses and identified enrichment of fluid shear stress and atherosclerosis (FSS-AS) signaling pathways in this subtype. The pachychoroid phenotype, together with FSS-AS enrichment, implicated altered choroidal hemodynamics in its pathogenesis. By inducing choroidal circulatory hypertension (CCH) in mice, we recapitulated, for the first time, the hallmark ocular lesions of pachychoroid PCV. Single-cell sequencing identified the cellular origin of these angiogenic lesions and implicated endothelin-1 (EDN1) as a key effector. Alleviating choroidal hypertension, reducing EDN1 expression, or pharmacologically blocking the endothelin receptor A (EDNRA, the receptor for EDN1), prevented lesion formation. In vitro, disturbed fluid shear stress upregulated EDN1 in choroidal endothelial cells and promoted pathological remodeling and angiogenesis through EDNRA. Collectively, our findings define a pathogenic cascade wherein CCH induces abnormal hemodynamics (disrupted fluid shear stress) and drives angiogenesis via the EDN1/EDNRA axis, offering mechanistic insight and identifying a potential therapeutic target for pachychoroid PCV.
-
3. {"_":"Different gut microbiome dysbioses impact the evolutionary fate of hypervirulent .","i":["Klebsiella pneumoniae"]}
3. 不同的肠道微生物组失调影响高毒力肺炎克雷伯菌的进化命运PMID:日期:2026-09-23The intestinal microbiota acts as a barrier against pathogen colonization, yet how specific ecological perturbations shape the evolutionary fate of invading pathogens remains unclear. Here, we show that the mode of gut perturbation and type of dysbiosis determine whether hypervirulent (hv) persist or clear from the intestines. Transient ampicillin exposure creates a permissive, low-diversity intestinal niche dominated by facultative anaerobes, which supports long-term, high-density hv colonization. The dysbiotic state creates an altered redox environment to favor these oxygen-using bacteria and is associated with the rapid emergence of hypomucoid variants. This occurs via contractions in the poly-T tract in the promoter of the regulator that controls capsule hypermucoviscosity, as well as mutations in the poly-G tract within the coding sequence. This evolutionary trajectory reflects a virulence-persistence trade-off in high-nutrient, low-competition environment. Conversely, osmotic perturbation via laxative treatment elicits only a transient window of colonization-susceptibility that is rapidly closed by the recovery of a -enriched community that is consistent with their ability to actively suppress pathogen colonization via short-chain fatty acids (SCFAs). Furthermore, SCFAs such as butyrate are more effective in inhibiting hypomucoid variants relative to wild-type bacteria, providing a possible explanation for how an osmotically perturbed gut microbiome constrains the expansion of these mutants. These findings provide insights into how transient antibiotic exposure could potentially drive long-term intestinal pathobiont colonization while laxative-induced osmotic perturbations do not rewire the energy and metabolic landscape of the gut microbiome, enabling rapid recovery and colonization resistance despite an initial plunge in diversity. Our work reveals that the specific mode of perturbation affects the trajectory for pathogen adaptation, and highlights the potential role of commensal competition in constraining pathogen evolution.
-
4. {"_":"Monocyte inflammation and adaptive immune dysfunction in severe pneumonia.","i":["Klebsiella pneumoniae"]}
4. {"_":"重症肺炎中的单核细胞炎症与适应性免疫功能障碍。","i":["肺炎克雷伯菌"]}PMID:日期:2026-09-21Severe pneumonia is associated with substantial mortality and is characterized by intense systemic inflammation that coexists with a failure to control infection. The cellular changes underlying the transition from effective host defense to immune dysfunction remain incompletely defined. Here, we constructed a severity-focused single-cell transcriptomic atlas of 708,894 peripheral blood mononuclear cells from 100 individuals (54 healthy controls, 23 patients with mild disease, and 23 patients with severe disease), complemented by plasma protein measurements and flow cytometry. Mild disease was characterized by a relatively coordinated peripheral immune response, with preserved monocyte regulatory and tissue-repair programs, preserved cytotoxic lymphocyte activity, and coordinated interactions between T follicular helper cells and B cells. Severe disease showed marked monocyte inflammation together with widespread disruption of adaptive immune responses. Classical monocytes expanded and showed increased expression of , accompanied by enhanced signaling and elevated plasma S100 proteins. These changes were accompanied by impaired dendritic cell antigen presentation, expansion of immunoregulatory monocyte states resembling monocytic myeloid-derived suppressor cells, cytotoxicity- and exhaustion-associated changes in CD8 T cells and natural killer cells, hyperactivated yet poorly coordinated CD4 T cell states, and weaker B cell receptor signaling despite plasma cell expansion. These findings delineate a severity-associated peripheral immune state characterized by monocyte-centered inflammatory signatures and features of altered adaptive immune coordination, and provide a basis for future mechanistic investigation of monocyte-derived alarmins and severity-associated myeloid remodeling.
-
5. {"_":"Gut derived leucic acid mediates the antiobesity effect of dietary fiber.","i":["Enterococcus faecium"]}
5. {"_":"肠道来源的白氨酸介导膳食纤维的抗肥胖作用。","i":["粪肠球菌"]}PMID:日期:2026-09-21Obesity is a globally prevalent metabolic disorder closely associated with gut microbiota dysbiosis. However, the precise roles of gut microbiota and microbial metabolism in this disease remain unclear. Through fecal metagenomic data mining and clinical cohort validation, we identified a gut bacterial strain with anti-obesity potential, (). It inhibited adipocyte enlargement, dyslipidemia, and hepatic steatosis in obese mice by metabolizing leucine to produce leucic acid (LEA). Colonization with or exogenous LEA supplementation improved obesity-associated metabolic phenotypes. Mechanistically, metabolized leucine into LEA via putative branched-chain amino acids metabolic enzymes. The bacterium-derived LEA regulated mitochondrial oxidative phosphorylation and thus alleviated obesity. Furthermore, using a high-content screening system and an in vitro fermentation model, we found that the dietary fiber glucomannan exerted anti-obesity effects by promoting the growth of . This study reveals the critical role of microbial metabolism and LEA production in ameliorating the onset and progression of obesity, providing a theoretical basis for dietary fiber intervention strategies targeting the gut microbiota.
-
6. Decoding sequence recognition code of nucleic acid-binding proteins of human-infecting DNA viruses.
6. 解码感染人类的DNA病毒核酸结合蛋白的序列识别密码PMID:日期:2026-09-08Human-infecting DNA viruses remain major health threats, yet the DNA-recognition mechanisms of their nucleic acid-binding proteins (NBPs) are poorly understood. Here, we systematically profiled 103 viral NBPs from human-infecting DNA viruses, with three NBPs from non-human-infecting DNA viruses as controls, using high-throughput screening. This analysis identified diverse DNA-binding motifs and specificity modules, including convergent recognition of a conserved CCACC motif across phylogenetically distant viruses. Notably, viral NBP binding-site distributions varied with genome size, and several NBPs from small-genome viruses showed enrichment on mitochondrial DNA. Functional assays further supported their mitochondrial association and effects on mitochondrial membrane potential. By integrating an ivTRT-based ssDNA-SELEX workflow, we further found that ssDNA viral NBPs recognize dimer-like and inverted-repeat sequences with potential to form stem-loop structures. Collectively, this study constructs a comprehensive viral NBP DNA-recognition atlas, offering a fundamental resource for elucidating viral genome recognition mechanisms, virus-mitochondria interactions, and developing future antiviral strategies.
-
7. Soil-derived, gut-dominant generalist bacteria shape the fitness of folivorous larvae.
7. 源自土壤、以肠道为主导的广食性细菌塑造了食叶幼虫的适合度PMID:日期:2026-08-30Whether Lepidoptera harbor a conserved core gut microbiome has long remained contentious. Through large-scale microbiome profiling of folivorous larvae, their host plants, and associated soils across three climatically distinct regions of China, we identify two soil-derived generalist bacteria, and sp., that colonize 97.92% of larval species examined, attaining mean relative abundances exceeding 47%, with the soil microbial reservoir as their principal source. Strikingly, these two taxa exhibit strong mutual exclusion within the larval gut yet govern host development through diametrically opposed metabolic strategies: promotes larval weight gain, whereas sp. suppresses growth. This functional bifurcation, in which two widespread generalists exert opposite phenotypic effects, represents a previously undescribed phenomenon in insect-microbe symbiosis. Our findings provide broad evidence that soil microbial reservoirs can shape aboveground herbivore fitness via horizontally acquired bacteria, offering mechanistic insights for microbiome-based ecological management.
-
8. Multi-omics-driven precision medicine.
8. 多组学驱动的精准医学PMID:日期:2026-08-25[中文摘要] 精准医学日益受到的制约，并非源于分子数据的缺乏，而是缺乏能够将多维生物学信息转化为可操作临床决策的框架。多组学驱动的精准医学（MODPM）通过将基因组学、表观基因组学、转录组学、蛋白质组学、代谢组学、微生物组和临床背景整合到一个多尺度框架中，将分子机制、组织结构和患者轨迹联系起来，从而弥补了这一不足。在本综述中，我们提出了MODPM的概念框架，并探讨了多组学技术、人工智能（AI）和基础模型的进步如何重塑疾病建模、药物开发和精准干预。我们总结了主要组学层面的生物学贡献，并讨论了AI如何支持跨模态表征学习、上下文建模和扰动感知预测。我们强调药物开发是MODPM的关键转化应用，并进一步讨论了其在三种主要疾病背景下的临床相关性：癌症、自身免疫性疾病和代谢性疾病，包括心脏代谢疾病和肾脏代谢疾病。这些例子说明了MODPM如何通过分析免疫失调、代谢重塑、慢性炎症、组织微环境变化和基因-环境相互作用等共享机制，支持靶点发现、疾病内型分型、治疗反应预测和临床监测。在这些场景中，MODPM能够实现更精细的分子分层、识别通路主导的疾病状态、改善反应预测以及动态治疗监测。我们还讨论了实施的关键障碍，包括数据异质性、队列多样性有限、多基因复杂性、工作流程限制、成本，以及与隐私、同意和数据所有权相关的伦理问题。总体而言，MODPM的价值不在于堆叠更多的数据层面，而在于构建一个多尺度、可持续学习的框架，将生物学异质性与临床可解释且可操作的决策联系起来。
[英文摘要] Precision medicine is increasingly constrained not by a lack of molecular data but by the absence of frameworks that can translate multidimensional biological information into actionable clinical decisions. Multi-omics-driven precision medicine (MODPM) addresses this lack by integrating genomics, epigenomics, transcriptomics, proteomics, metabolomics, microbiome, and clinical context into a multiscale framework that links molecular mechanisms, tissue organization, and patient trajectories. In this review, we propose a conceptual framework for MODPM and examine how advances in multi-omics technologies, artificial intelligence (AI), and foundation models are reshaping disease modeling, drug development, and precision intervention. We summarize the biological contributions of major omics layers and discuss how AI supports cross-modal representation learning, contextual modeling, and perturbation-aware prediction. We highlight drug development as a key translational application of MODPM and further discuss its clinical relevance across three major disease contexts: cancer, autoimmune diseases, and metabolic disorders, including cardiometabolic and renal-metabolic diseases. These examples illustrate how MODPM can support target discovery, disease endotyping, treatment response prediction, and clinical monitoring by analyzing shared mechanisms such as immune dysregulation, metabolic remodeling, chronic inflammation, tissue microenvironmental changes, and gene-environment interactions. Across these settings, MODPM enables finer molecular stratification, the identification of pathway-dominant disease states, improved response prediction, and dynamic treatment monitoring. We also discuss key barriers to implementation, including data heterogeneity, limited cohort diversity, polygenic complexity, workflow constraints, cost, and ethical issues related to privacy, consent, and data ownership. Overall, the value of MODPM lies not in stacking additional data layers but in building a multiscale, continuously learnable framework to link biological heterogeneity to clinically interpretable and actionable decisions.
-
9. The gut microbiome organ.
9. 肠道微生物组器官PMID:日期:2026-08-21The human gut microbiome is increasingly viewed as an active regulator of host physiology, extending beyond earlier taxonomy-centered descriptions of a complex microbial community. Accumulating evidence supports an organ-like conceptual framework in which the gut microbiome exhibits spatially structured organization, extensive metabolic capacity, and continuous bidirectional communication with host systems. Through the production of bioactive metabolites with endocrine-like, immunomodulatory, and neuromodulatory properties, the microbiome contributes to metabolic, immune, and neuroendocrine regulation, thereby influencing systemic homeostasis and disease susceptibility. Recent advances in multi-omics, spatial biology, and computational modeling are moving the field from taxonomic association toward functional interpretation, mechanistic insight, and causal inference. These approaches are beginning to reveal microbiome-derived functional modules and host-microbe signaling networks that are shaped by host genetics, diet, medications, feeding patterns, circadian rhythms, and environmental exposures. In this review, we synthesize current mechanistic and translational evidence to conceptualize the gut microbiome as an organ-like functional system, delineate its structural and functional organization, and propose a framework for mapping, modeling, and therapeutically targeting microbiome-derived circuits to support precision medicine in metabolic, inflammatory, and selected gut-brain axis-related disorders.
-
10. Human biomarker navigator.
10. 人类生物标志物导航器PMID:日期:2026-08-20Biomarkers play a pivotal role in contemporary medical research, particularly in the early diagnosis of diseases and personalized treatment. Although previous studies have systematically reviewed markers across various disease domains, an integrated framework that connects major physiological systems, encompasses multiple organs, and spans a broad spectrum of diseases is still lacking. In the context of modern health challenges, marked by the high prevalence of chronic diseases and widespread comorbidities, establishing a panoramic biomarker navigation system is imperative. This review offers the initial comprehensive elucidation of the biomarker interaction networks across diverse systems, organs, and diseases, and delineates the operational framework for establishing a "biomarker navigation system". The core contribution of this work is a transition from 'knowledge enumeration' to a more integrated, systems-level approach. This provides new perspectives in systems biology for understanding the shared pathological foundations of comorbidities. Furthermore, it provides a theoretical basis for a reorientation in medicine, from a focus on 'treating existing diseases' to 'preventive interventions' and from 'single-disease management' to a comprehensive, systems-based approach. To facilitate the exploration and application of this system-organ-disease-biomarker network, we developed the "Human Biomarker Navigator" web platform (http://www.hbiomarker.com), which allows researchers and clinicians to efficiently retrieve the functional characteristics and clinical significance of diverse biomarkers across different disease contexts.