International Journal of Stem Cells国际干细胞杂志
International Journal of Stem Cells(英文缩写 INT J STEM CELLS),ISSN 2005-3606,eISSN 2005-5447,中文译名:国际干细胞杂志 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：2025-10-01 至 2026-09-30，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 |
|---|---|---|
| 2021 | 3.011 | Q4 |
| 2022 | 2.300 | Q4 |
| 2023 | 2.500 | Q3 |
| 2024 | 2.400 | Q4 |
| 2025 | 2.600 | Q3 |
International Journal of Stem Cells 最新收录文献
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1. Hyperbaric Oxygen Treatment Enhances Definitive Endoderm Differentiation and Hepatic Maturation of Human-Induced Pluripotent Stem Cells in Association with mTORC2-Dependent AKT Phosphorylation.
PMID:日期:2026-09-17Hepatocyte-like cells derived from human-induced pluripotent stem cells (hiPSCs) are widely used in disease modeling, drug screening, and regenerative medicine. However, efficient generation of mature hepatocyte-like cells from hiPSCs remains challenging. In this study, we investigated whether hyperbaric oxygen treatment (HBOT) during the definitive endoderm (DE) differentiation process enhances DE induction and subsequent hepatocyte maturation. hiPSCs were exposed to HBOT 1∼3 times during a 4-day DE differentiation protocol. Among these, two HBOT sessions most effectively increased the expression of DE-specific markers, including SRY-box transcription factor 17, GATA binding protein 4, forkhead box A2, and C-X-C motif chemokine receptor 4 (CXCR4). Flow cytometry revealed that HBOT increased both the proportion of CXCR4-positive DE cells and the mean CXCR4 fluorescence intensity. Mechanistically, HBOT-induced phosphorylation of protein kinase B (AKT) at serine 473, which was not completely inhibited by phosphoinositide 3-kinase but was reduced by Torin2 treatment. This suggests that AKT activation induced by HBOT is associated with a mechanistic target of rapamycin complex 2-dependent pathway. Furthermore, DE cells generated under HBOT conditions produced hepatocyte-like cells exhibiting increased expression of hepatic markers, such as albumin, alpha-fetoprotein, hepatocyte nuclear factor 4 alpha, and asialoglycoprotein receptor 1. Collectively, these results demonstrate that HBOT enhances DE induction efficiency during the early differentiation stage and promotes the generation of more mature hiPSC-derived hepatocyte-like cells. The findings suggest that HBOT can be a useful physical regulatory strategy to improve hiPSC-based hepatocyte differentiation protocols.
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2. Optimization of a Canine Colon Organoid Platform for Modeling Intestinal Injury and Mesenchymal Stem Cell-Mediated Regeneration.
PMID:日期:2026-08-25Canine chronic enteropathy (CE) is characterized by persistent mucosal inflammation and impaired barrier function. Despite its high clinical prevalence, research has been hindered by a lack of host-specific intestinal models. Here, we present an optimized canine-derived colon organoid (cCO) culture platform designed for assessing drug toxicity and regenerative potential. Combining Wnt/EGF activation with TGF-β/p38 MAPK inhibition supported the long-term maintenance of stem cell-enriched organoids. Upon maturation, differentiated cCOs exhibited both absorptive and secretory cells, validated by lineage-specific marker expression and functional P-glycoprotein efflux activity. While pro-inflammatory cytokines exerted non-specific toxicity, diclofenac-induced injury was significantly more pronounced in differentiated organoids than in expanding counterparts. This indicates that our platform effectively recapitulates the cell type-specific sensitivity of the intestinal epithelium to pharmacological insults. Next, to determine whether the cCOs could model epithelial repair process, we examined the therapeutic effects of canine mesenchymal stem cells (MSCs), a representative cell-based therapy for CE, on damaged organoids. Notably, treatment with MSC-conditioned media (MSC-CM) triggered a morphological transition into cystic spheroids with the upregulation of pro-regenerative stem cell markers, suggesting the induction of a fetal-like regenerative reprogramming. Indeed, MSC-CM treatment restored growth and proliferation while preserving barrier integrity in diclofenac-treated organoids. Collectively, these findings demonstrate the advantages of cCO system for modeling intestinal injury and repair, supporting the development of targeted therapeutic strategies for canine gastrointestinal disorders.
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3. Therapeutic Effect of Pioglitazone-Pretreated Human Wharton's Jelly-Derived Mesenchymal Stem Cells in a Rat Tendon Injury Model.
PMID:日期:2026-08-21The clinical application of mesenchymal stem cells (MSCs) has several limitations owing to their less therapeutic efficacy. Effect enhancement and MSCs from new sources might help in overcoming these limitations. The aim of the present study was to investigate the therapeutic effects of human Wharton's jelly-derived MSCs (hWJMSCs) and pioglitazone-pretreated MSCs (Pio-MSCs) in a rat tendon injury model. Fifty-four Sprague Dawley rats were randomly assigned to three groups: phosphate-buffered saline (PBS) group, implanted with PBS; MSC group, implanted with MSCs; and Pio-MSC group, implanted with Pio-MSCs. The cell or PBS with fibrin glue mixture was implanted around bilateral window defect in the Achilles tendons of the rats. The cross-sectional area measurement, histological analysis, gene expression, protein expression, and biomechanical analysis were performed at 2 and 4 weeks after modeling. Pio-MSC group revealed a significantly higher gene expression level of than PBS group at 2 weeks and that of at 2 and 4 weeks. Moreover, MSC group revealed significantly higher gene expression level of than PBS group at 2 weeks. In general, the expression levels of and were the highest in Pio-MSC group, followed by MSC and PBS groups. Furthermore, Pio-MSC group revealed significantly higher tenascin C-stained fraction than PBS group at 4 weeks. These findings suggest a potential role of hWJMSCs in tendon regeneration; however, the enhancement effect of pioglitazone pretreatment over MSC alone was not confirmed, and no differences were observed in histological or biomechanical outcomes among the groups.
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4. Efficacy and Safety of Low-Molecular-Weight Collagen Peptide GT for Improving Hair Condition in Individuals with Damaged Hair: A Randomized, Double-Blind, Placebo-Controlled Trial.
PMID:日期:2026-08-21Addressing hair damage is essential for maintaining overall hair and scalp health. Previous studies have suggested that low-molecular-weight collagen peptides may support hair follicle biology through regulation of extracellular matrix homeostasis and cellular signaling pathways. In addition, recent preclinical studies have demonstrated that low-molecular-weight fish collagen peptides promote hair regrowth through activation of proliferative signaling and suppression of inhibitory pathways. However, their clinical efficacy in improving hair damage has not been clearly established. In this study, the efficacy and safety of low-molecular-weight collagen peptide GT (LMWCP GT) were evaluated in Korean adults with damaged hair. In a randomized, placebo-controlled trial, individuals aged 19∼60 years without alopecia but with mild to moderate hair damage received LMWCP GT (3 g/day) for 24 weeks. Compared with placebo, the treatment group demonstrated significant improvements in hair gloss, as measured using a gloss meter (SAMBA) and scanning electron microscopy, as well as in hair elasticity, assessed by tensile strength and hair diameter. Subjective evaluations further indicated improvements in overall hair condition, including gloss, elasticity, thickness, texture, fullness, and appearance. In addition, scalp elasticity was significantly increased in the treatment group. No treatment-related adverse events were observed. These findings indicate that daily supplementation with LMWCP GT (3 g/day) for 24 weeks is safe and effective in improving overall hair condition in individuals with damaged hair without alopecia.
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5. Human-Relevant Microphysiological Systems: Evidence for Defined Contexts of Use.
PMID:日期:2026-08-20The FDA Modernization Act has accelerated the transition from animal-based testing toward human-relevant new approach methodologies in drug development, shifting attention from technological feasibility to regulatory implementation. Among these approaches, microphysiological systems (MPS) can generate evidence that more directly reflects human physiology, but their regulatory readiness varies substantially across applications. This Review summarizes recent regulatory developments and evaluates the readiness of major organ-specific and multi-organ MPS. Liver MPS have advanced furthest through quantitative benchmarking, industrial adoption and sustained regulatory engagement, whereas kidney, lung, gastrointestinal, tumor, nervous system and multi-organ models remain limited by varying degrees of standardization, independent validation and clearly defined regulatory use. Across applications, major barriers include insufficiently specified contexts of use, limited human benchmark data, inadequate multicenter reproducibility, manufacturing variability and fragmented data infrastructure. We discuss priorities for overcoming these barriers, including performance-based standards, quality-controlled manufacturing, auditable data systems and earlier coordination among technology developers, end users and regulatory authorities. Patient-derived and stem cell-derived models, artificial intelligence and digital twins may further extend the scope of MPS, but their value will depend on transparent validation and integration with complementary evidence. Regulatory adoption is likely to proceed incrementally, with MPS initially supporting defined decisions as complementary evidence and replacing conventional studies when their performance and uncertainty are sufficiently characterized.
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6. Fibroblast Growth Factor Signaling in Lung Diseases: From Biological Roles to Therapeutic Delivery Strategies.
6. 肺疾病中的成纤维细胞生长因子信号传导：从生物学作用到治疗传递策略PMID:日期:2026-08-07As human longevity continues to increase globally, the prevalence of age-related deterioration and associated chronic lung diseases has risen in parallel. Unlike many organs, the lung is continuously exposed to environmental insults, leading to cumulative cellular damage, impaired epithelial progenitor activity, and chronic inflammation, which contribute to diseases such as pulmonary fibrosis and chronic obstructive pulmonary disease. Under physiological conditions, lung homeostasis is maintained by epithelial progenitor cells, particularly alveolar type II cells. However, this regenerative capacity is often disrupted in chronic lung diseases, resulting in impaired repair and fibrotic remodeling. Fibroblast growth factors (FGFs) and their receptors (FGFRs) play critical roles in epithelial regeneration, cell survival, and tissue repair. Despite their therapeutic potential, clinical translation remains limited by poor protein stability, rapid proteolytic degradation, low delivery efficiency across biological barriers, and insufficient cell-type specificity due to broad FGFR expression. Recently, several delivery strategies have been evaluated in preclinical lung disease models, including protein engineering, nanoparticle and liposome-based platforms, protein transduction domain- and cell-penetrating peptide-based intracellular delivery, and mesenchymal stem cell-based approaches. Therefore, this review summarizes the roles of FGF signaling in lung regeneration and age-associated diseases, and discusses emerging delivery strategies aimed at bridging the gap between preclinical efficacy and clinical application.
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7. Lineage-Driven Understanding of Human Pericyte Heterogeneity in Vascular Modeling and Regeneration.
PMID:日期:2026-08-04Pericytes are mural cells embedded within the microvascular wall that regulate endothelial stabilization, angiogenesis, and vascular permeability. Once regarded as a relatively uniform vascular support population, pericytes are now recognized as quantitatively and functionally heterogeneous across organs. Neural barrier beds such as brain and retina exhibit high pericyte density and near-continuous mural coverage, whereas peripheral tissues including skeletal muscle display sparse investment. These anatomical differences parallel functional specialization, with central nervous system pericytes exerting strong control over blood-brain barrier (BBB) integrity and transcytosis, while peripheral pericytes participate prominently in vascular remodeling and repair. A critical yet under-integrated dimension of this heterogeneity is developmental origin. Trunk and visceral pericytes arise predominantly from mesodermal progenitors, whereas cranial and forebrain-associated pericytes derive largely from neural crest lineage. This spatial segregation of embryonic origin aligns with vascular specialization, suggesting that lineage contributes to mural regulatory architecture. Stem cell-based comparisons further demonstrate that neural crest-derived pericyte-like cells induce BBB phenotypes more effectively than mesoderm-derived counterparts under identical endothelial conditions, supporting a lineage-linked functional bias. This review integrates anatomical distribution, quantitative investment patterns, molecular signaling mechanisms, and embryonic lineage into a unified framework of pericyte heterogeneity. We propose that developmental origin establishes a regulatory foundation upon which vascular niche signals act, and should therefore be treated as a primary experimental and translational design variable in vascular modeling and regenerative strategies.
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8. {"_":"A Cerebral Organoid Model of Familial Alzheimer's Disease Using Amyloid Precursor Protein Mutation, Val669Leu ().","i":[{"_":"APP","sup":["Seoul"]}]}
8. 使用淀粉样前体蛋白突变的家族性阿尔茨海默病的脑类器官模型，Val669Leu（APPSeoul）PMID:日期:2026-07-29Various animal and cellular Alzheimer's disease (AD) models harboring familial AD (fAD) mutations have been developed and widely used for AD research. In this study, we established an AD cerebral organoid (CO) model using a novel Val669Leu () mutation in the APP gene. We generated a human embryonic stem cell (hESC) line overexpressing , referred to as the fAD-S hESC line. Using this line, we produced COs and confirmed robust AD-associated pathologies, including amyloid- (A) accumulation and tau phosphorylation. In addition, increased expression of -secretase was observed in this model. Based on these findings, we investigated the effects of BACE1 inhibitor IV, a -secretase inhibitor, in the CO model. Treatment with BACE1 inhibitor IV significantly reduced A levels and tau phosphorylation. Furthermore, we differentiated the fAD-S hESC line into cortical neurons (fAD-S neurons) to establish a 2D cellular AD model. Consistent with the CO results, fAD-S neurons exhibited elevated levels of A and phosphorylated tau, which were also significantly attenuated by BACE1 inhibitor IV treatment. Collectively, these results demonstrate the successful establishment of hESC-derived 2D and 3D AD models based on the fAD mutation.
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9. CXCL14 Enhances Myocyte Fusion and Activates the FAK-ERK5 Signaling Pathway in Skeletal Muscle Stem Cells and Myoblasts.
PMID:日期:2026-07-29Skeletal muscle regeneration is essential for maintaining muscle function throughout life and is regulated by numerous growth factors, cytokines and their associated signaling pathways. In this study, we investigated the role of C-X-C motif chemokine ligand 14 (CXCL14) in myogenic differentiation using skeletal muscle stem cells (MuSC) and the mouse myoblast C2C12 cell line. Notably, CXCL14 significantly enhanced myocyte fusion. To elucidate the underlying regulatory mechanisms, we examined fusion-associated signaling pathways and found that CXCL14 activates the focal adhesion kinase-extracellular regulated protein kinase 5 (FAK-ERK5) signaling pathway. Our findings identify the CXCL14-FAK-ERK5 signaling axis as a positive regulator of myocyte fusion. Furthermore, by establishing fibro-adipogenic progenitors (FAPs) as the primary source of CXCL14 and demonstrating its pro-fusion activity, this study provides new insight into the paracrine regulation from FAPs to MuSCs during muscle regeneration.
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10. Recent Advances in Genetically Engineered Mouse Models of Melanoma: Insights into Tumor Initiation and Oncogenic Signaling Pathways.
PMID:日期:2026-07-23Genetically engineered mouse (GEM) models are essential for elucidating the cellular and molecular mechanisms underlying various human diseases. Because mouse skin closely resembles the structure and lineage organization of human skin, melanoma GEM models enable the investigation of melanoma initiation in melanocytes and melanocyte stem cells, along with its progression from the epidermis to the dermis. Although early melanoma development is mainly regulated by major oncogenic signaling pathways, including MAPK and PI3K, recent studies have uncovered additional regulatory pathways, including Cdk4-mediated cell-cycle control, Jak-Stat-mediated transcriptional regulation, Hippo-Yap/Taz signaling, the p62-Igf2bp1 axis, and epigenetic regulators such as Tet2, which contribute to melanoma heterogeneity and phenotypic plasticity. This review summarizes the recent advances in melanoma GEM models, highlights the oncogenic signaling pathways active in these systems, and discusses the molecular insights derived from these models regarding melanoma initiation, progression, and intratumoral diversity. These findings highlight the utility of GEM models for elucidating melanoma biology and identifying potential therapeutic targets.