International Review of Cell and Molecular Biology国际细胞与分子生物学评论
International Review of Cell and Molecular Biology,ISSN 1937-6448,eISSN N/A,中文译名:国际细胞与分子生物学评论 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 |
|---|---|---|
| 2020 | 6.813 | Q1 |
| 2021 | 6.420 | Q1 |
International Review of Cell and Molecular Biology 最新收录文献
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1. Mitophagy's impact on obesity-related tissues.
PMID:日期:2026-01-01Obesity, a global health crisis, results from an energy imbalance, leading to metabolic dysfunction and associated conditions such as type 2 diabetes, cardiovascular disease, and metabolic dysfunction-associated steatotic liver disease. A strong link exists between obesity and mitochondrial dysfunction, characterized by reduced mitochondrial mass, impaired oxidative capacity, and decreased ATP production. Mitophagy, a specific type of autophagy targeting mitochondria for degradation, plays a complex, tissue-specific role in regulating metabolism and mitigating the harmful effects of obesity. Both insufficient and excessive mitophagy can negatively influence disease progression. In white adipose tissue, mitophagy functions as a quality control mechanism that reduces oxidative stress and helps maintain insulin sensitivity. However, chronic obesity impairs mitophagy due to overactivation of mTORC1 and inhibition of AMPK, leading to inflammation and insulin resistance. In brown adipose tissue, mitophagy is essential for thermogenesis and energy expenditure, but excessive activation in obesity may impair thermogenesis. In the liver, mitophagy is crucial for preserving mitochondrial function and preventing metabolic dysfunction-associated steatotic liver disease. In the heart, mitophagy supports cardiac function, particularly in obesity-related cardiomyopathy. In skeletal muscle, obesity worsens impairments in mitochondrial quality control, disrupting the clearance of damaged mitochondria. Therefore, there is a pressing need for therapies that restore mitophagic balance in a context- and depot-specific manner, as the dysregulation of mitophagy contributes not only to local dysfunction but also to broader metabolic phenotypes.
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2. Autophagy meets plant virology: From molecular crosstalk to outstanding challenges.
PMID:日期:2026-01-01Autophagy is an evolutionarily conserved degradation and recycling pathway that plays essential roles in plant development, stress adaptation, and immunity. Over the past decade, increasing evidence has revealed that autophagy also shapes the outcome of plant-virus interactions. This review summarizes current understanding of the plant autophagy machinery as well as the experimental approaches used to monitor autophagic flux during viral infection. We then explore the diverse roles of autophagy in the plant-virus interface, highlighting its function as an antiviral mechanism that targets viral components for degradation, and the counterstrategies viruses employ to inhibit or evade this defense. Conversely, some viruses exploit autophagy or its components to facilitate replication, movement, or systemic infection, underscoring its dual nature in plant virology. Recent studies have expanded knowledge of selective autophagy receptors that mediate targeted degradation of viral factors, yet the diversity and specificity of these receptors are likely far from fully characterized. Finally, we discuss outstanding questions such as the mechanisms underlying virus-induced autophagy, the factors determining its switch between antiviral and proviral roles, its crosstalk with other cellular pathways, and the molecular signatures that guide the selective recognition of viral or host proteins. Overall, autophagy emerges as an important regulatory hub in plant-virus interactions, integrating antiviral defense and viral adaptation in a finely tuned balance.
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3. Sex matters in macroautophagy: Sex-driven differences in autophagic function in aging and aging related-diseases.
PMID:日期:2026-01-01Autophagy is a fundamental cellular process essential for maintaining homeostasis, particularly in the context of aging and age-related diseases. Increasing evidence highlights biological sex as a critical modulator of autophagy, influencing its basal activity, regulatory pathways, and responsiveness to stress. Distinct autophagic profiles in males and females (across tissues, species and developmental stages) may underlie sex-specific vulnerabilities and divergent disease trajectories. These differences are evident in conditions such as neurodegeneration, cardiovascular disease, cancer, sarcopenia or chronic inflammation, all of which are commonly associated with aging. Indeed, aging is a major risk factor for the onset and progression of these pathologies. Importantly, sex-dependent variations in autophagy might also impact the efficacy and safety of therapeutic interventions, challenging the validity of uniform treatment strategies. Despite growing recognition of these disparities, significant knowledge gaps remain. This review summarizes current understanding of sex-related differences in autophagy, focusing on genetic and hormonal influences across the lifespan. The evidence supports the need for future research to systematically incorporate sex as a biological variable in experimental design and data analysis, utilize dynamic assessments of autophagy flux and investigate the interplay among genetic, hormonal, epigenetic, and post-translational regulatory mechanisms. Developing preclinical models that reflect human diversity-including genetic heterogeneity and relevant hormonal states-is imperative. Embracing the complexity of sex-dependent autophagy regulation is essential for translating mechanistic insights into effective, personalized interventions that improve health outcomes for both women and men.
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4. Viral trafficking: The role of autophagy in the release of virus-loaded extracellular vesicles.
PMID:日期:2026-01-01Over the past decade, the interplay between autophagy process and viral replication, alongside the mechanisms by which viruses evade immune surveillance, has been extensively investigated. Increasing evidence indicates that viruses hijack the autophagic machinery to facilitate the release of extracellular vesicles (EVs) carrying viral components. This involvement highlights autophagy as a central hub in viral trafficking, bridging intracellular remodelling with extracellular dissemination. In this review, we explore how viruses exploit autophagy and EV pathways to promote replication and enable non-lytic release. We highlight the molecular interactions underlying EV biogenesis and secretory autophagy and discuss the emerging potential of EVs as biomarkers and therapeutic platforms, despite current technical challenges. Finally, we examine strategies to target the autophagy-EV interface as an antiviral strategy.
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5. Autophagy in endothelial cells: A gatekeeper of immune cell trafficking and function.
PMID:日期:2026-01-01Endothelial cells (ECs) are increasingly recognised as dynamic regulators of immunity rather than passive vascular barriers. By integrating inflammatory, metabolic, and mechanical cues, ECs actively shape leukocyte trafficking and determine inflammatory outcomes. Autophagy, a conserved lysosomal degradation pathway essential for cellular homeostasis, has emerged as a key determinant of endothelial function in health and disease. Recent work identifies EC autophagy as a context-dependent determinant of leukocyte trafficking, vascular inflammation, antigen presentation, and endothelial phagocytic capacity. Beyond controlling immune cell recruitment, EC autophagy intersects with xenophagy, efferocytosis, and vascular ageing, highlighting its broad immunomodulatory potential. In this review, we synthesise current evidence defining how autophagy within ECs regulates immune responses in a tissue-specific manner during acute and chronic inflammation. Collectively, these insights position EC autophagy as a central integrator of vascular and immune homeostasis and underscore its potential as a therapeutic target in chronic inflammatory and ageing-associated diseases.
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6. Lysosomal function and homeostasis: From cellular adaptation to disease pathogenesis.
PMID:日期:2026-01-01Lysosomes were once considered terminal degradative organelles responsible for disposing of cellular waste. However, recent studies have revealed that lysosomes serve as dynamic signalling and metabolic hubs at the center of diverse biological processes, including nutrient sensing, metabolic regulation, membrane trafficking, autophagy, inflammation, and cell death. To support this broad functional repertoire, lysosomes must possess robust mechanisms to maintain their integrity in the face of damage or stress. In response to lysosomal membrane damage, cells engage multilayered adaptive mechanisms that act in coordination-membrane repair (Repair), selective removal of damaged organelles (Removal), and de novo biogenesis of lysosomes (Regeneration). These processes are mediated by a range of molecular pathways, including the ESCRT complex, the PITT pathway, lysophagy, and TFEB-dependent lysosomal regeneration. Notably, recent findings highlight the noncanonical autophagy-like pathway known as ATG8ylation (conjugation of ATG8s on single membranes), which is activated via the STING-V-ATPase-ATG16L1 axis and functions as a critical hub connecting multiple arms of the lysosomal damage response. In this review, we systematically outline the molecular basis of lysosomal damage responses, including ATG8ylation, and explore how these networks are implicated in a broad spectrum of pathological conditions such as aging, neurodegeneration, cancer, obesity-related disorders, and immune dysfunction. Understanding these lysosomal quality control mechanisms not only sheds light on the fundamental principles of organelle homeostasis but also opens new avenues for therapeutic innovation.
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7. Advances in nano biomaterials for biomedical engineering.
PMID:日期:2026-01-01Systemic toxicity and off target effects are some of the major drawbacks of traditional, broad-spectrum therapies. Nanotechnology effectively counters these by offering precise, targeted alternatives and hence, reshaping biomedical engineering, therapeutics, diagnostics and even tissue regeneration. We explore six key nano-biomaterial platforms that exemplify this technological revolution. Silk fibroin nano-patches with engineered exosomes help diabetic wounds heal by producing collagen. Hydrogel activated with nanoparticle form nanoadhesives that bond well with wet environments, such as surgical sites. Graphene-based neural interfaces are characterized by high electrical conductivity with low immunogenicity. Bioelectronic-hydrogel composites adapt tissue mechanics for better physiological sensing. The pH-responsive metal-organic frameworks show remarkable potential in cancer treatment enabling targeted drug delivery, reducing harm to surrounding healthy tissue, and magnetic nanoparticles coated in cancer cell membranes improve natural killer-cell therapies. Despite these remarkable advances, the challenge of transition from laboratories to clinics faces many hurdles. Demands for scalable manufacturing techniques, strategies to suppress undesirable immune reactions and passing through safety and regulatory standards are some of the major challenges in Nanotechnology. Collaborative approaches from interdisciplinary fields like material science, biology, engineering and clinics may present a positive outlook to these issues. Nanotechnology can offer promising precision medicine tailored to an individual's safety and dosage profiles, minimising off target interaction risks.
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8. MRI acute/sub-acute ischemic stroke segmentation with deep learning: A comprehensive review.
PMID:日期:2026-01-01The segmentation of ischemic stroke lesions from Magnetic Resonance Imaging (MRI) images using deep learning (DL) techniques has emerged as a critical area of research in medical imaging. This article provides a comprehensive review of the current state-of-the-art methodologies in this domain, focusing on the advancements and challenges inherent in this field. Our review focuses on studies that utilize DL models for segmenting acute and sub-acute ischemic stroke lesions using MRI modalities. By systematically analyzing research from 2020 onward, we aim to clarify the advancements in the published models' effectiveness and provide a performance benchmark. This review stands out by comprehensively analyzing all the studies in this field, beyond the scope of prior reviews focused only on key publications. Additionally, this work serves as a comprehensive reference for researchers by compiling all relevant datasets, MRI modalities, evaluation metrics, loss functions, input data dimensionality, preprocessing, and augmentation techniques employed for this task. Additionally, we identify the challenges in this field and highlight the existing research gaps, in addition to proposing some directions for future work to enhance the effectiveness and accuracy of DL models in stroke lesion segmentation.
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9. Bioink-based 3D bioprinting: Paving the path for regenerative medicine.
9. 基于生物链的3D生物打印：为再生医学铺平道路PMID:日期:2026-01-01Three-dimensional (3D) bioprinting has come a long way to have emerged as a transformative technology in bio-fabrication. Bioinks with specific attributes of cellular compatibility, mechanical strength, printability, and biodegradability remain crucial factors and yet a critical challenge. More growth in bioinks is happening with 4D bioprinting due to new developments in supramolecular hydrogels and both naturally and artificially made polymers. iPSCs, organ-on-chip technologies, and microfluidics allow scientists to produce sensitive tissue used for drug therapy and diagnosing diseases. Extrusion, inkjet, and stereolithographic printing let 3D bio-printers mix several materials, preserve cells, and create highly detailed prints. Despite the differences and similarities of AI and automation, they can both be valuable for ensuring quality control. Concerns that limit the clinical use of 3D bioprinting involve regulations, the uneven consistency of bioink, and the importance of ensuring long-term security. It is essential to develop platforms for bioprinting that are scalable, reasonably low-cost, and GMP-compliant and to maintain close collaboration among different fields to achieve all that personalized regenerative medicine and clinical care for cancer, heart disease, neurological diseases, and similar illnesses can offer.
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10. Advances in ferroptosis research and applications.
10. 铁下垂病的研究和应用进展PMID:日期:2026-01-01Ferroptosis is an iron-dependent form of regulated cell death driven by lipid peroxidation and redox imbalance. It has emerged as a pivotal mechanism implicated in various diseases, including cancer, chronic kidney diseases (CKD), neurodegenerative disorders, pulmonary fibrosis, chronic wounds, and viral infections such as COVID-19. This chapter presents a comprehensive overview of the molecular underpinnings of ferroptosis, emphasizing its key regulators-iron metabolism, lipid peroxidation pathways, and antioxidant defenses such as GPX4 and system Xc. We explore recent advances highlighting the therapeutic potential of ferroptosis modulation across multiple pathological contexts. In cancer, ferroptosis inducers have shown efficacy in overcoming drug resistance and enhancing immunotherapy. In contrast, inhibition of ferroptosis offers protective effects in neurodegenerative diseases, ischemia-reperfusion injury, and chronic inflammatory conditions. Applications in nanomedicine have further enabled targeted delivery of ferroptosis modulators, expanding their clinical relevance. The chapter also discusses emerging roles of ferroptosis in wound healing, CKD and pulmonary fibrosis, with particular attention to COVID-19-related lung injury. Finally, we evaluate current therapeutic strategies, safety considerations, and potential clinical applications, along with future directions including biomarker development and personalized medicine. Our aim is to provide a unified perspective on ferroptosis as a disease-modifying mechanism and to highlight its growing importance as a therapeutic target across diverse clinical disciplines.