TRENDS IN MOLECULAR MEDICINE分子医学趋势

TRENDS IN MOLECULAR MEDICINE(英文缩写 TRENDS MOL MED),ISSN 1471-4914,eISSN 1471-499X,中文译名:分子医学趋势 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
18.100
JCR 分区
Q1
CAS 分区
B1
近一年发文量
157
本站 PubMed 收录统计

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。

ISSN: 1471-4914 · eISSN: 1471-499X · 缩写: TRENDS MOL MED ·中文: 分子医学趋势

期刊介绍

选择期刊介绍栏目

期刊简介

《Trends in Molecular Medicine》是Cell Press旗下综述型期刊,聚焦分子医学领域的前沿进展,连接基础分子生物学与临床疾病机制。主要覆盖疾病分子基础、靶点发现、转化医学及新型治疗策略,读者群为分子医学、生物医学与临床转化方向的研究人员、医师科学家及高年级研究生。

研究方向

期刊发表分子层面疾病机制、遗传与表观遗传调控、免疫与代谢通路、肿瘤及神经退行性疾病等方向的综述、观点与短评,也接受少量原创研究。论文类型以邀请综述为主,强调对已有证据的整合与概念提炼,而非单纯数据报告。

期刊特色

研究取向偏重机制整合与转化前景,论文通常由领域内活跃学者撰写,图表精炼、观点鲜明,适合希望快速把握某一分子医学方向全貌并寻找交叉切入点的读者。对临床医生和基础研究者均有参考价值。

投稿难度

投稿难度较高,通常需先与编辑沟通选题并获邀约,自由来稿接受率有限。准备时应突出概念创新与领域争议,避免文献罗列;若为原创研究,需有明确分子机制和转化意义。建议先阅读近期同主题综述,评估差异化定位。

历年影响因子趋势

JCR 数据年份影响因子JCR 分区
202115.272Q1
202213.600Q1
202312.800Q1
202413.800Q1
202518.100Q1

TRENDS IN MOLECULAR MEDICINE 最新收录文献

  1. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    1. Genomic newborn screening, a healthcare system transformation.

    作者:
    Lilian Downie, Zornitza Stark
    日期:
    2026-09-23

    Genomics has revolutionised the diagnosis of rare diseases and is now set to transform prevention through integration with newborn screening programmes. This will identify a broader range of severe, treatable diseases while creating the potential for data reuse across the lifetime. However, for effective population-wide implementation, a shift in the healthcare system to support preventive rather than reactive healthcare will need to occur. In addition, potential harms need to be identified and minimised. This review covers key components of this system shift including parental consent and choice, data workflows and reporting, education, and health-economic impact. Utilising digital technology and global collaboration will be integral to successful evidence generation at scale and to the integration of genomics into public health.

  2. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    2. The splicing axis of aging: mechanisms and therapeutic opportunities.

    作者:
    Sada Raza, Ankita Kumari, Maciej Cieśla
    日期:
    2026-09-21

    Aging is characterized by progressive loss of molecular fidelity that compromises stem-cell function and tissue homeostasis. Aging transcriptomes show widespread disruption of RNA processing, including increased intron retention, cryptic splice-site usage, and altered RNA quality control. These changes arise from somatic mutations as well as accumulated transcriptional, metabolic, and proteostatic stress. Importantly, similar splicing abnormalities are observed in age-associated diseases such as clonal hematopoiesis and neurodegeneration, overlapping with physiological aging states. Here, we synthesize mechanistic, stem-cell, and longevity studies to define declining RNA-processing fidelity as a unifying contributor to aging across systems. We propose the 'splicing axis of aging' as a framework linking RNA-processing dysfunction to tissue decline and outline emerging therapeutic strategies to restore spliceosome integrity and RNA homeostasis.

  3. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    3. Pulsatile farnesoid X receptor activation rewires liver disease pharmacology.

    作者:
    Guangyuan Zhao, Yufan Rao, Pengfei Xu
    日期:
    2026-09-15

    Nuclear receptor agonists face a dilemma: sustained receptor activation improves efficacy but inevitably exacerbates mechanism-based toxicity. Zang et al. challenge this by demonstrating that transient, physiologically synchronized farnesoid X receptor activation maintains efficacy while minimizing adverse effects, introducing temporal control of signaling as a new precision-therapeutic paradigm.

  4. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    4. hPSC models in cancer mechanisms and therapeutic discovery.

    作者:
    Chih-Wei Chu, Yen-Tzu Chang, Candise Tat, Rachel Shoemaker, Dung-Fang Lee
    日期:
    2026-09-15

    Despite major advances in cancer genomics and immunotherapy, the field remains limited by experimental models that fail to faithfully recapitulate human tumor initiation, genetic context, and immune-tumor interactions. Traditional animal and immortalized cell models often lack predictive power for therapeutic response and toxicity. Recent advances in human pluripotent stem cell (hPSC) technology have transformed this landscape, enabling the generation of patient-specific cancer models, multicellular organoids and assembloids, and scalable immune effector cells. These platforms now permit mechanistic dissection of tumorigenesis, reconstruction of human tumor microenvironments, and development of off-the-shelf immunotherapies. This review will synthesize these emerging findings, define key technological and biological gaps, and outline future directions for integrating hPSC-based modeling into precision oncology and translational cancer research.

  5. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    5. Extracellular vesicles redefine glioma detection.

    作者:
    Viktoria Szydlik, Patricia Sanchez-Rojas, Irene Rebollido-Pedrido, Petra Hamerlik
    日期:
    2026-09-03

    Robinson et al. challenge the reliance on neurosurgery for glioma diagnosis by integrating multi-omic profiling of plasma extracellular vesicles with machine learning. Across independent cohorts, these biomarkers discriminate between glioma and controls and enable longitudinal tracking of tumor burden, establishing a clinically relevant foundation for minimally invasive diagnosis, monitoring, and stratification.

  6. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    6. The niche-metabolism axis: reprogramming tumor-associated macrophages for precision immunotherapy.

    作者:
    Lijun Zhao, Xuyun Li, Wenyue Liu, Wanru Zhao, Miao Qi, Meiqi Lin, Tao Zhang, Baile Zuo, Huilong Yin, Junjie Li, Angang Yang, Rui Zhang
    日期:
    2026-08-18

    Tumor-associated macrophages (TAMs) critically modulate solid tumor progression and immunotherapy resistance, yet their profound context-dependent heterogeneity defies the traditional M1/M2 dichotomy. In this review, we propose the 'niche-metabolism axis' framework, deconstructing the tumor microenvironment into dynamically interacting functional niches (e.g., hypoxic cores and tertiary lymphoid structures). Within these niches, specific physicochemical stresses substantially influence localized TAM metabolic reprogramming. Metabolites such as lactate and lipids act not merely as substrates but as signaling mediators and epigenetic donors, shaping TAM phenotypes. Consequently, TAMs acquire spatial metabolic imprints and evolve into 'ecosystem engineers' that actively remodel the immune microenvironment. This framework highlights that therapeutic paradigms should shift from nonselective TAM depletion to niche-specific metabolic-epigenetic reconstruction, providing a precise roadmap for designing next-generation engineered macrophage therapies.

  7. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    7. Emerging therapeutic opportunities targeting nonclassical MHC-I molecules.

    作者:
    Yan-Ruide Li, Yuning Chen, Lili Yang
    日期:
    2026-08-17

    Nonclassical major histocompatibility complex class I (MHC-I) molecules, including human leukocyte antigen E (HLA-E), HLA-F, HLA-G, MHC-I-related protein 1 (MR1), and the CD1 family, constitute a conserved antigen-presenting system that regulates immune surveillance, tissue homeostasis, and tolerance through specialized interactions with innate and unconventional T cells. Although these molecules have long been implicated in cancer, infection, autoimmunity, and transplantation, their distinct immunobiology and therapeutic potential have largely been considered in isolation. Recent advances in structural immunology, single-cell and spatial profiling, engineered immune cell technologies, and early clinical studies have established nonclassical MHC-I pathways as tractable targets for immunotherapy. In this review, we synthesize the biology, disease-associated functions, and therapeutic targeting of these molecules, integrating immune checkpoint blockade, antibody-based therapeutics, and MR1- and CD1-restricted cellular immunotherapies into a unified framework. We further highlight shared immunological principles, emerging clinical translation, and opportunities for universal, off-the-shelf immune interventions.

  8. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    8. Formicitoxins: membrane-targeting antifungal peptides from carpenter ant venoms.

    作者:
    Wei Zhang, Melina Sarabandi, Vinit Kumar
    日期:
    2026-08-14

    Fungal infections cause millions of deaths, yet clinical antifungals span only three drug classes. Koch et al. discover formicitoxins-35 venom peptides from carpenter ants-which are the first from any formicine species. Two outperform voriconazole in vitro and delay infection in vivo. Formicitoxins disrupt fungal membranes independently of existing drug targets.

  9. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    9. RNA translational control in skeletal development, homeostasis, and disease.

    9. 骨骼发育、稳态和疾病中的RNA翻译调控
    作者:
    Denghao Huang, Siyuan Hu, Qiwen Li, Quan Yuan
    日期:
    2026-08-14

    [中文摘要] 骨骼的发育、维持与修复需要精确控制蛋白质的生成,然而mRNA水平往往与蛋白质丰度相关性较差。翻译是将mRNA转化为蛋白质的过程,但其在骨骼生物学中的作用远不如转录调控那样被充分理解。近年来翻译组学(translatomics)的进展开始揭示翻译调控如何参与骨骼发育、稳态与修复。本文总结了跨骨骼谱系、发育阶段及疾病状态下的翻译控制,并讨论了研究mRNA翻译的新兴方法以及靶向翻译通路的潜在治疗机会。理解翻译调控如何塑造骨骼健康与疾病,将为骨骼缺陷的精准干预开辟新途径。

    [英文摘要] Skeletal development, maintenance, and repair require precise control of protein production, yet mRNA levels often correlate poorly with protein abundance. Translation is the process through which mRNA is converted into protein, but its role in skeletal biology remains much less understood than that of transcriptional regulation. Recent advances in translatomics have begun to reveal how translational regulation contributes to skeletal development, homeostasis, and repair. Here, we summarize translational control across skeletal lineages, developmental stages, and disease settings. We also discuss emerging approaches for studying mRNA translation and potential therapeutic opportunities that target translational pathways. Understanding how translational regulation shapes skeletal health and disease will open new avenues for precise interventions for skeletal defects.

  10. JCR分区: Q1 CAS分区: B1 影响因子: 18.1

    10. Tumor metaboception: local PGE2 signals global decline.

    作者:
    Ming-Zhu Jin, Hao-Ran Dang, Wei-Lin Jin
    日期:
    2026-08-13

    Cancer cachexia has long been attributed to circulating factors. Cross et al. now show that, in liver kinase B1 (Lkb1)-mutant lung tumors, local prostaglandin E2 acts on vagal neurons to drive anorexia and wasting, accelerated by fat. Defining metaboception as neural sensing of local signals-a new therapeutic concept.

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