SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY细胞与发育生物学专题综述

SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY(英文缩写 SEMIN CELL DEV BIOL),ISSN 1084-9521,eISSN 1096-3634,中文译名:细胞与发育生物学专题综述 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。

2026 年数据 · 影响因子
6.700
JCR 分区
Q1
CAS 分区
B2
近一年发文量
37
本站 PubMed 收录统计

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。

ISSN: 1084-9521 · eISSN: 1096-3634 · 缩写: SEMIN CELL DEV BIOL ·中文: 细胞与发育生物学专题综述

期刊介绍

选择期刊介绍栏目

期刊简介

Seminars in Cell & Developmental Biology 是一本以专题综述为主的国际期刊,聚焦细胞生物学与发育生物学的前沿进展。每期围绕一个特定主题,邀请领域内专家撰写综述,系统梳理机制、模型与争议。读者主要为细胞与发育领域的研究人员、研究生及教学人员,适合快速了解某一方向的整体图景与关键问题。

研究方向

主要覆盖细胞信号转导、细胞周期与分化、干细胞与再生、胚胎发育与模式形成、细胞器动态、细胞死亡与代谢调控等方向。论文类型以邀约综述和专题合辑为主,也包含少量观点与展望类文章,强调对已有证据的整合与概念提炼,而非原始实验数据。

期刊特色

研究取向偏重机制整合与跨方向比较,文章通常由活跃在该专题的学者撰写,结构清晰、引用较全,便于读者建立知识框架。适合已具备一定背景、希望追踪热点或寻找课题切入点的研究者,也适合作为研究生课程阅读材料。

投稿难度

投稿难度中等偏上,通常以编辑邀约为主,自由投稿需先与编辑沟通选题。准备时应突出专题的新颖性与整合价值,避免与近期综述重复,并明确目标读者与核心问题。不能仅凭分区或影响因子判断是否容易录用,选题契合度和综述质量更为关键。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
20217.499Q1
20227.300Q1
20236.200Q1
20246.000Q1
20256.700Q1

SEMINARS IN CELL & DEVELOPMENTAL BIOLOGY 最新收录文献

  1. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    1. Change of fate: How do gall-inducing insects redirect plant developmental programs to create new organs?

    作者:
    Jack C Schultz, Graham N Stone
    日期:
    2026-09-23

    Many insects elicit development of unique organs in their host plants called galls while feeding or ovipositing. Galls are organ-like entities that protect against biotic and abiotic stresses and provide a specialized nutrition supply. The signals used by gall-forming insects to elicit and shape galls are unknown, but phytohormones, peptides, small RNAs and arabinogalactan proteins are leading candidates. These four signal categories may work together to elicit galls and guide their development, but evidence of their transfer from insect to plant is incomplete. Galls vary in complexity from simple swellings to elaborate organs and their morphologies are tightly linked to the insect's identity. The attacked host plant tissue also shapes the gall's development, especially via physical constraint. The interaction between insect signaling and tissue constraints on development makes insect behavior important for establishing and shaping the gall. Because plant tissues are heterogeneous mosaics of cells with differing transcriptomes that change with time, galling insects must locate specific plant cells at specific points in their development to initiate their characteristic galls. Experimental evidence of signal transfer and function in planta, time series records of cell behavior during gall development, and single-cell plant tissue transcriptome maps would provide a fuller understanding of the galling phenomenon.

  2. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    2. Keeping up with the neighbors: Coordinating cell fate within and across epidermal layers.

    作者:
    Mauna Musulchi, Katie Cockburn
    日期:
    2026-09-15

    Stratified epithelia such as the skin epidermis face a formidable challenge: maintaining a functional barrier in the face of continuous cellular turnover. Coping with this challenge means that keratinocytes must be exquisitely sensitive to the identity, position, and behavior of their neighbors. This review highlights emerging work on how cell fates are coordinated across the layers of the interfollicular epidermis during homeostatic regeneration, with a particular focus on how density changes, local signaling patterns, and mechanical cues control progenitor behaviors in the basal layer and facilitate the ordered progression of terminal differentiation in the suprabasal layers above.

  3. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    3. Energetic constraints on growth across biological scales.

    作者:
    Youmna Atieh, Thomas Lecuit
    日期:
    2026-09-10

    Growth requires the continuous conversion of environmental resources into biomass and usable energy. Despite the high energetic efficiency of oxidative phosphorylation, the ability of cells and organisms to expand metabolism during growth is constrained by multiple physical and physiological factors. Increasing evidence suggests that metabolic strategies during growth are shaped not solely by energetic efficiency but by a series of constraints operating across biological scales: environmental factors such as temperature and oxygen availability impose external limits on metabolic demand and supply. At the organismal level, transport networks constrain the distribution of oxygen and nutrients. Within cells, geometric scaling, membrane allocation limits, biosynthetic capacity, and proteome investment restrict oxidative metabolism. Finally, recent thermodynamic analyses suggest that these diverse constraints may converge on a more general limit on free energy dissipation by cells. Together, these perspectives support the view that energetic constraints not only limit growth but actively shape how growth is achieved across biological scales. Under such constraints, cells frequently adopt alternative metabolic strategies, mainly increased reliance on fermentative pathways. Integrating energetic constraints across scales provides a unified framework for understanding metabolic strategies during growth.

  4. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    4. Dysplastic basal-like cells in alveolar repair and regeneration.

    作者:
    Tiantian Lu, Lian Xie, Claude Jourdan Le Saux, Harold A Chapman, Ying Xi
    日期:
    2026-09-01

    The lung is constantly exposed to environmental insults, leading to the evolution of diverse repair mechanisms that involve regional stem and progenitor cells. However, in response to severe alveolar injury, aberrant basal-like cells emerge in the alveolar regions, as observed in acute viral infections and chronic pulmonary diseases like lung fibrosis. While these cells can rapidly reseal the epithelial barrier, they fail to restore normal lung function and, if persistent, represent dysplastic repair. This review summarizes recent advances in understanding the cellular origin, regulation, and function of these basal-like cells. Elucidating how dysplastic repair arises and mechanistically links to alveolar regeneration and disease progression will provide insights into the mechanism of regeneration failure in chronic lung diseases and help inform the development of potential therapies.

  5. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    5. Mitochondrial dynamics and mechanosignalling - Integrating metabolic demand and life-death decisions with microenvironmental mechanics.

    作者:
    Fabianna Tennant, Andrew P Gilmore
    日期:
    2026-09-01

    The way by which cells sense and interpret their microenvironment is fundamental to the regulation of their behaviour. Mechanosignalling is an essential aspect of microenvironmental sensing by cells, particularly within complex three-dimensional tissues, but it remains unclear how this signalling interacts with and modulates organelles such as mitochondria. Mitochondria form a dynamic network throughout the cytoplasm, intricately intertwined with the cytoskeleton and other organelles such as the endoplasmic reticulum. The complex coregulation of these networks controls how cells respond to dynamic changes in metabolic demand. Recent studies have shown that mitochondrial networks are acutely sensitive to mechanosignalling, but it remains in question whether they respond directly to contractile forces from the cytoskeleton or if their reorganisation occurs downstream of broader metabolic reprogramming. Here we discuss recent work highlighting the complexity in understanding this.

  6. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    6. Biosynthetic solutions to mechanical stress: why do mechanical stresses drive altered metabolism?

    作者:
    Allen Lee, Isabel Sakowicz, Cray Minor, Anton V Block, Kolade Adebowale, Kevin M Tharp
    日期:
    2026-09-01

    Cells reside in mechanically stressful microenvironments where protrusive and traction forces from neighboring cells and cell-intrinsic forces derived from adhesions to the extracellular matrix (ECM) establish a dynamical "Mechanoreciprocity". Mechanoreciprocity is the concept that cells respond to the physical properties of the cellular microenvironment by reciprocally exerting proportional forces [1]. However, if feed-forward mechanical stress responses based on energetically demanding cytoskeletal dynamics are the only ways cells reciprocally respond to physical cues, we would not observe the force-induced thickening of bone [2] or hypertension-associated collagen accumulation in the kidney [3]. These processes are examples of adaptive biosynthetic responses by cells that may serve to buffer mechanical stresses in energetically efficient ways. In this review, we will introduce some of the ways in which cells respond to the physical properties of the microenvironment and suppose why these observed metabolic changes serve to support biosynthetic solutions to buffer mechanical stresses, a response that can preserve tissue structure or, in excess, distort it.

  7. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    7. The trypanosome flagellum as model for parasitology, cell biology and ciliopathies.

    作者:
    Amandine Hecquet, Serge Bonnefoy, Philippe Bastin
    日期:
    2026-09-01

    Cilia and flagella exhibit widely conserved structures and functions across species. In humans, defects in these organelles are responsible for diseases called ciliopathies and many model organisms are used to study them. In this review, we will discuss one of them, the parasite Trypanosoma brucei, which is particularly well-suited to investigate general aspects of cilia and flagella, such as construction or protein localisation. Its flagellum remains present throughout the cell cycle, offering the opportunity to monitor flagellum maintenance and assembly within the same cell. This model organism is very convenient for flagellum live imaging as well as expansion microscopy and ultrastructural studies, including focused ion beam - scanning electron microscopy (FIB-SEM). Efficient tools exist to manipulate the genome, including endogenous tagging, inducible expression system, RNA interference and CRISPR-Cas9 approaches. Here, we review original contributions from studies in trypanosome to our understanding of flagellum construction and intraflagellar transport, as well as the impact of gene mutations in some ciliopathies.

  8. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    8. A metabolic view of gastrulation: Coordinating signalling, epigenetics and morphogenesis.

    作者:
    Tatiana Firfa, Tamara Civetta, Eunice HoYee Chan, Kristina S Stapornwongkul
    日期:
    2026-09-01

    Gastrulation is the morphogenetic process by which the single-layered pluripotent epiblast is reorganised into the three germ layers and the basic body plan is established. While the metabolic state of pluripotent stem cells is well characterised, the metabolic remodelling that coincides with germ layer specification is less well understood. Emerging evidence suggests that metabolism functions as more than a passive housekeeping process and instead acts as a dynamic regulator of cell state during these developmental transitions. Here, we review recent work that implicates a role for metabolic pathways in regulating cell fate and morphogenesis during gastrulation. In particular, glucose metabolism appears to serve as a critical regulatory layer, modulating morphogen signalling to promote the emergence and function of mesodermal and endodermal populations. We also discuss the role of the tricarboxylic acid cycle and one-carbon metabolism in epigenetic remodelling and highlight the role of lipid metabolism in coupling the biophysical properties of membranes to cellular identity and morphogenetic movements. A current challenge is to distinguish in which situations metabolic shifts act as instructive drivers or permissive gatekeepers of development. Technological advances in spatial metabolomics, biosensors, and optogenetics are now facilitating the visualisation and manipulation of metabolic activity, paving the way for a mechanistic understanding of how metabolism shapes cell fate and behaviour during gastrulation.

  9. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    9. Manipulation of biological systems by self-defecting and foreign agents.

    作者:
    Evgeniya V Shmeleva, Michael Levin
    日期:
    2026-09-01

    Biological systems maintain structure and function through hierarchical control, redundancy and surveillance across scales. These same features create leverage points for agents that establish a persistent presence in host systems, including foreign agents such as pathogens, parasites, trophoblasts and gall-inducing insects, and self-defecting agents such as cancer. This review synthesises evidence across immunology, developmental biology, neuroscience, oncology and ecology to treat manipulation as a staged control problem in which local access is converted into distributed effects through shared signalling and feedback loops across scales. We outline a six-step framework in which manipulators establish access, interfere with boundary and identity checks, exploit transient plasticity to reset homeostatic constraints, redirect immune, endocrine and neural communication, remodel host structure through developmental programmes, and stabilise altered states through niche construction and epigenetic remodelling. The framework separates mechanisms required for initiation from those required for maintenance and long-term persistence. We illustrate this framework through four case studies: trophoblast invasion in pregnancy, tumour progression, parasitoid manipulation by Cotesia congregata, and plant galls. The synthesis highlights recurrent vulnerabilities in boundaries, shared signalling and plasticity windows, and motivates stage-specific experiments that test whether candidate mechanisms drive entry, sustain the manipulated state, or increase resistance to reversal. The same logic can help organise thinking about complex pathology in which altered states are maintained by distributed feedback.

  10. JCR分区: Q1 CAS分区: B2 影响因子: 6.7

    10. Nutrient-sensing pathways in adult stem cells: Orchestrating homeostasis, aging, and disease.

    10. 成体干细胞中的营养感应途径:协调稳态、衰老和疾病
    作者:
    Tianxiong Xiao, Zhiyao Xie, Lijun Yao, Ke Zhao, Yi Arial Zeng, Cheng Hu
    日期:
    2026-09-01

    Nutrient-sensing pathways, including mTOR, AMPK, Sirtuins, and insulin/IGF-1 signaling, are central regulators orchestrating adult stem cell (ASC) fate by dynamically modulating cellular metabolism. This review proposes a framework that integrates these pathways into a cohesive network that dictates the metabolic transitions between quiescence, activation, and differentiation in ASCs. Age-related dysregulation of this network leads to metabolic imbalance and stem cell exhaustion, underpinning tissue degeneration. Interventions such as mTOR inhibitors, AMPK activators, NAD precursors, and dietary strategies can rejuvenate ASC function by restoring metabolic balance, underscoring their therapeutic potential for mitigating aging and associated diseases.

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