FASEB JOURNAL
FASEB JOURNAL(英文缩写 FASEB J),ISSN 0892-6638,eISSN 1530-6860 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 |
|---|---|---|
| 2021 | 5.834 | Q1 |
| 2022 | 4.800 | Q1 |
| 2023 | 4.400 | Q1 |
| 2024 | 4.200 | Q1 |
| 2025 | 4.300 | Q1 |
FASEB JOURNAL 最新收录文献
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1. Hypoxia Combined With Substance P Pretreatment of ADSC-Exos Promotes Recruitment and Differentiation of EPCs by Activating YAP/TEAD3 to Treat Diabetic Foot Ulcer.
PMID:期刊:日期:2026-10-05Diabetic ulcers are associated with high amputation and mortality rates, significantly impacting patients' life quality. Both hypoxia and substance P (SP) treated-ADSC-Exos promote wound healing and angiogenesis in diabetic foot ulcers. However, the effects of combined hypoxia and SP pretreatment remain unclear. ADSCs were isolated and treated with hypoxia and SP, and then ADSC-Exos were extracted and identified. A diabetic foot ulcer mice model was established and treated with hypoxia plus SP preconditioned ADSC-Exos. Wound area and the expression of CD31 and CD34 in the gastrocnemius muscle were assessed. Endothelial progenitor cells (EPCs) were isolated from healthy and diabetic mice, and the migration capacity, differentiation potential, and tubule formation ability were evaluated. CXCR4 expression in ADSC, ADSC-Exos, and EPCs treated with ADSC-Exos was measured. TFDB prediction, ChIP, and dual-luciferase assays were used to explore TEAD3 transcriptional regulation of CXCR4. ADSC-Exos were isolated successfully. Hypoxia plus SP preconditioned ADSC-Exos improved wound healing and angiogenesis in diabetic mice. In vitro, they also promoted EPC migration, endothelial differentiation, and tube formation. The expression of CXCR4 increased in ADSC and ADSC-Exos treated with hypoxia plus SP, and surface CXCR4 was elevated in EPCs. Knockdown of CXCR4 counteracted the pro-angiogenic effects of hypoxia plus SP treated ADSC-Exos in diabetic mice. Mechanistically, hypoxia/SP activated YAP signaling, promoting TEAD3-mediated transcription of CXCR4, while inhibition of YAP-TEAD interaction reduced CXCR4 expression. Hypoxia combined with SP promotes CXCR4 expression in ADSCs by activating the YAP/TEAD3 signaling pathway, thereby increasing CXCR4 levels in ADSC-Exos, and finally promotes the recruitment and differentiation of EPCs to treat diabetic foot ulcer.
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2. Time-Dependent Efficacy of Lymphaticovenous Anastomosis in Secondary Lymphedema: A Rabbit Model Study.
2. 淋巴静脉吻合术治疗继发性淋巴水肿的时效性疗效：一项兔模型研究PMID:期刊:日期:2026-10-05Secondary lymphedema remains a common complication after oncologic lymph node dissection. The optimal timing of lymphaticovenous anastomosis (LVA) is unclear due to a lack of time-dependent large-animal models. Twenty-five New Zealand White rabbits underwent popliteal-region surgery to induce secondary hind limb lymphedema. Animals received immediate LVA (n = 5) or delayed LVA at 4, 8, or 12 weeks after model induction (n = 5 per group); untreated lymphedema controls were included (n = 5). Outcomes included limb circumference/swelling rate, anastomotic patency by indocyanine green (ICG) fluorescence imaging, and histopathology/molecular markers (e.g., VEGF-C, LYVE-1). The model produced sustained hind limb swelling and molecular evidence of lymphangiogenic remodeling (e.g., increased VEGF-C and LYVE-1). Immediate LVA achieved 100% technical success with durable patency during follow-up. Delayed LVA groups demonstrated patency rates of approximately 75%-80%. Immediate intervention resulted in the greatest long-term reduction in swelling compared with delayed interventions. Mean lymphatic and venous diameters were approximately 0.6 and 0.8 mm, respectively, and mean operative time was ~55 min. This rabbit model provides a reproducible platform to evaluate time-dependent LVA efficacy. Earlier intervention yielded superior functional outcomes, while delayed LVA remained feasible and maintained reasonable patency, supporting a clinically relevant therapeutic window.
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3. The Genetic and Epigenetic Mechanisms of mtDNA in Regulation of Inflammation and Metabolism.
3. mtDNA在炎症和代谢调节中的遗传和表观遗传机制PMID:期刊:日期:2026-10-05Mitochondria serve as the primary cellular powerhouses, generating ATP through oxidative phosphorylation (OXPHOS) to sustain essential cellular processes. Beyond energy production, mitochondria function as critical regulators of metabolic homeostasis, intracellular signaling networks, and programmed cell death pathways. The mitochondrial genome comprises 37 genes encoding 13 OXPHOS subunits, 22 transfer RNAs, and 2 ribosomal RNAs, all transcribed and translated within the organelle. Mitochondrial DNA integrity becomes compromised through diverse pathological stimuli, including metabolic dysregulation, oxidative stress, and inflammatory cascades, contributing to disease pathogenesis across multiple organ systems. This review synthesizes current knowledge on the multifaceted roles of mtDNA in health and disease. We propose a framework of three interconnected mechanisms through which mtDNA exerts its effects: (1) retrograde signaling to the nucleus, reprogramming nuclear gene expression; (2) cytosolic and extracellular release of mtDNA as a damage-associated molecular pattern (DAMP), activating innate immune pathways like cGAS-STING and NLRP3; and (3) intrinsic epigenetic modifications that directly modulate mitochondrial gene expression. We critically evaluate the evidence linking mtDNA alterations to a spectrum of diseases, including cancer, cardiovascular and metabolic disorders, neurodegeneration, and psychiatric conditions. We conclude that a comprehensive understanding of mtDNA's multifaceted nature, moving beyond its perception as a mere DAMP, is essential for translating mitochondrial biology into effective clinical interventions.
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4. Estrogen Receptor Beta Isoforms Interplay Integrates Nuclear and Extra-Nuclear Signaling to Modulate Human Granulosa Cell Growth.
4. 雌激素受体β亚型相互作用整合核内与核外信号传导以调控人颗粒细胞生长PMID:期刊:日期:2026-10-03Estradiol (E2) regulates ovarian follicular development and granulosa cell (GC) function primarily through estrogen receptor β (ERβ). Human GCs express several ERβ isoforms, including ERβ1, ERβ2, ERβ4, and ERβ5, but how their relative abundance modulates estrogen signaling remains unclear. Here, we investigated the contribution of nuclear and extra-nuclear ERβ signaling to human GC growth and function. HGrC1 granulosa cells lacking endogenous estrogen receptors were engineered to stably express individual or combined ERβ isoforms. Functional analyses showed that ERβ1 and ERβ4 inhibited GC proliferation, whereas ERβ2 and ERβ5 promoted cell growth. Co-expression of all isoforms resulted in an overall inhibitory effect, indicating that GC responses depend on ERβ isoform balance rather than a single receptor. Reporter assays demonstrated that only ERβ1 activated estrogen response element-dependent transcription, while the other isoforms suppressed E2-dependent ERα transactivation. In contrast, ERβ2, ERβ4, and ERβ5 activated AP-1 signaling in a ligand-independent manner and attenuated ERβ1-mediated repression, identifying AP-1 as a central node of ERβ isoform crosstalk. RNA sequencing following selective ERβ1 depletion in primary human granulosa lutein cells revealed that ERβ1 is required for E2 responsiveness and regulates genes involved in membrane potential, ion transport, and cytoskeletal organization. Proteomic and biochemical analyses further identified isoform-specific signaling networks involving ERK1/2, Akt, and CaMKII pathways. Together, these findings demonstrate that ERβ isoform balance orchestrates estrogen signaling through coordinated nuclear and extra-nuclear mechanisms controlling GC growth and function.
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5. Combination of Empagliflozin and Resveratrol Mitigates Hepatic Steatosis via Attenuation of Inflammation and Promotion of Adipose Tissue Browning in High-Fat Diet-Fed C57BL/6J Mice.
5. 恩格列净与白藜芦醇联合用药通过减轻炎症和促进脂肪组织棕色化缓解高脂饮食喂养C57BL/6J小鼠的肝脏脂肪变性PMID:期刊:日期:2026-10-02Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major hepatic complication of obesity with a complex pathogenesis. This study aims to investigate the combined effects of empagliflozin (EMPA) and resveratrol (RSV) treatment on obesity-associated MASLD in a high-fat diet (HFD)-fed mouse model. C57BL/6J mice were fed by HFD for 23 weeks, along with treatment with EMPA (0.01% w/w), RSV (0.4% w/w), and their combination. Metabolic parameters, glucose tolerance, hepatic steatosis, inflammation, and adipose tissue morphology and function were evaluated using biochemical assays, histology, immunofluorescence, qPCR, western blotting, and F-FDG PET scan. Combination therapy reduced body weight gain and improved glucose tolerance more effectively than monotherapies. It significantly alleviated hepatic steatosis, as shown by decreased liver weight, triglyceride content, MASLD activity score (MAS), and serum ALT/AST levels. Co-treatment also reduced hepatic inflammation by suppressing macrophage infiltration, shifting macrophages toward an M2 anti-inflammatory phenotype, inhibiting NF-κB activation, and enhancing AMPK phosphorylation. Furthermore, the combination more effectively activated brown adipose tissue thermogenesis and induced browning in subcutaneous white adipose tissue, evidenced by upregulation of UCP1, PGC-1α, TFAM, and TMEM26, increased mitochondrial biogenesis, and enhanced cold tolerance. The combination of EMPA and RSV exerts a multi-targeted therapeutic effect against HFD-induced MASLD. This combination represents a promising novel strategy for MASLD prevention.
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6. Physiological Responses to Intermittent Environmental Heat Stress in Mice.
6. 小鼠对间歇性环境热应激的生理反应PMID:期刊:日期:2026-10-02Environmental heat stress is an emerging ecological problem, yet the physiological mechanisms linking repeated heat exposure to cardiovascular disease risk remain incompletely understood. Here, we investigated the systemic, cardiovascular, metabolic, and immune consequences of intermittent environmental heat stress. C57BL/6J Mice were exposed to intermittent hyperthermia (30°C-37°C, 3 h/day, 4 days/week) for up to four weeks under controlled environmental conditions. The core body temperature, blood pressure, and endothelial activation were measured by SoHo telemetry devices, tail-cuff, and intravital microscopy, respectively. During heat exposure (> 33°C) there was a level dependent increase in core body temperature and water and food intake exposures. Exposure to 37°C elicited a robust neuroendocrine stress response characterized by a 2-4-fold increase in plasma corticosterone levels, > 50% reductions in plasma epinephrine, and a robust induction of heat shock proteins in the vasculature. Heat exposure also transiently reduced systolic and diastolic blood pressure by ~10 mmHg and > 30% depletion in circulating immune cell populations. Despite this systemic leukopenia, repeated heat stress (37°C, 3 h/day, 4 days/week, 4-weeks) increased leukocyte rolling and adhesion to the vascular endothelium (> 3-fold), indicative of enhanced endothelial activation. In contrast, repeated heat exposure had minimal effects on cardiac systolic function, arterial stiffness, plasma lipid levels, or markers of overt organ injury. These findings demonstrate that repeated environmental heat stress induces coordinated neuroendocrine, vascular, immune, and metabolic adaptations characterized by activation of heat shock pathways, immune remodeling, and endothelial activation that precede cardiovascular dysfunction.
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7. Establishment of an Animal Model of Type 2 Cardiorenal Syndrome.
7. 2型心肾综合征动物模型的建立PMID:期刊:日期:2026-10-02Type 2 cardiorenal syndrome (CRS) is a complex clinical syndrome characterized by chronic kidney injury resulting from chronic cardiac dysfunction. Its underlying pathophysiological mechanisms remain incompletely understood, highlighting the urgent need for disease models that better mimic human pathology and accurately simulate the progression of cardiac-induced renal injury. Existing models possess significant limitations and often fail to adequately replicate the onset and progression observed in clinical Type 2 CRS patients. We therefore hypothesized that a double-hit approach combining left anterior descending (LAD) ligation (to induce acute myocardial infarction) with transverse aortic constriction (TAC) (to increase afterload) would produce a model that highly simulates the development and progression of clinical Type 2 CRS, characterized by heart failure and subsequent renal injury. A double-hit strategy combining LAD ligation and TAC was performed in mice to induce heart failure followed by secondary renal injury. At four post-operative time points (2 weeks, 4 weeks, 6 weeks, and 8 weeks), we assessed cardiac function, renal function, inflammatory damage, energy metabolism dysfunction, and renal/cardiac fibrosis. Proteomic analysis was additionally performed to characterize molecular changes and identify the optimal model configuration. At week 2, mice developed early-stage heart failure accompanied by mild kidney inflammation and abnormal energy metabolism. By week 4, these abnormalities progressed to marked inflammation, fibrosis, chronic heart failure, and overt kidney damage. The impairments in energy metabolism, inflammation, and fibrosis peaked at Weeks 6 and 8, leading to severe dysfunction of both the heart and kidneys. This double-hit model stably recapitulates the natural progression from chronic cardiac dysfunction to chronic kidney injury observed in Type 2 CRS. It therefore serves as a powerful and innovative research platform for in-depth exploration of the molecular mechanisms underlying Type 2 CRS, screening of potential therapeutic targets, and evaluation of novel interventional strategies.
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8. Hepatic Sialylation Defects Increase Susceptibility to Obesity and Steatosis in Mice.
PMID:期刊:日期:2026-10-02Sialic acid is a well-characterized monosaccharide known to regulate early development and lifelong health, and its aberrant metabolism has been closely linked to multiple pathologies including cancer, cardiovascular disease, and neurological disorders. However, its role in early-life metabolic programming and adult metabolic homeostasis remains poorly understood. Here, we investigated Cmp-Neu5Ac synthase (CMAS), a key enzyme in the sialylation pathway, using two complementary mouse models to address this gap. In a mammary-specific Cmas knockout model, reduced milk sialyllactose levels significantly altered offspring metabolic development. Offspring nursed by CMAS-deficient dams displayed increased body weight and impaired glucose and insulin tolerance at weaning. When challenged with a high-fat diet, these offspring developed exaggerated weight gain, enhanced adipose expansion, and more severe hepatic ballooning degeneration, indicating that early-life sialylation deficiency disrupts metabolic programming and increases susceptibility to metabolic stress in adulthood. To determine whether sialylation is also essential for maintaining hepatic metabolic stability later in life, we generated a liver-specific Cmas knockout model. Deletion of Cmas markedly reduced serum sialylation and hepatic Neu5Gc-containing glycopeptides, leading to hepatomegaly, steatosis, and fibrosis, which was accompanied by activated lipogenic axis, impaired mitochondrial respiratory complex activity, increased mitochondrial fission and triggered compensatory AMPK-PGC1α signaling. Notably, CMAS deficiency sensitized hepatocytes to inflammatory stress, as evidenced by exacerbated lipid accumulation, elevated ROS production, and reduced ATP content upon LPS challenge. Together, our results demonstrate that sialylation is indispensable for both developmental metabolic programming and adult hepatic metabolic homeostasis, establishing a critical link between sialylation status and lifelong metabolic health.
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9. RETRACTION: Epstein-Barr Virus-Encoded miR-BART6-3p Inhibits Cancer Cell Proliferation Through the LOC553103-STMN1 Axis.
9. 撤稿：爱泼斯坦-巴尔病毒编码的miR-BART6-3p通过LOC553103-STMN1轴抑制癌细胞增殖PMID:期刊:日期:2026-10-02D. Wang, Z. Zeng, S. Zhang, F. Xiong, B. He, Y. Wu, W. Li, L. Tang, F. Wei, B. Xiang, Z. Li, Y. Zhou, M. Zhou, X. Li, Y. Li, G. Li, W. Xiong and C. Guo, "Epstein-Barr Virus-Encoded miR-BART6-3p Inhibits Cancer Cell Proliferation Through the LOC553103-STMN1 Axis," The FASEB Journal 34, no. 6 (2020): 8012-8027, https://doi.org/10.1096/fj.202000039RR. The above article, published online on 18 April 2020 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Loren E. Wold; the Federation of American Societies for Experimental Biology; and Wiley Periodicals, LLC. The journal received allegations by a third party of image reuse and relabeling within the same paper and across other publications by a subset of the authors. Further investigation of the article by the publisher confirmed the third-party concerns and detected evidence of additional image reuse and relabeling. Specifically, multiple immunoblot panels in Figure 3A, Figure 3B, Figure 3C, and Figure 5B were reused throughout the paper. In addition, an immunoblot panel in Figure 3A and Figure 5B was reused from an earlier publication. The retraction has been agreed to because of the evidence of image duplication in multiple figures and across papers, which fundamentally compromises the editors' confidence in the conclusions presented. The authors did not respond when asked to agree to the final wording of the retraction.
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10. Endothelial Exostosin-1 Is Needed for Glycocalyx Integrity and Inflammatory Resolution in Acute Lung Injury.
PMID:期刊:日期:2026-10-01The endothelial glycocalyx depends on Exostosin-1 (Ext1)-mediated heparan sulfate synthesis; however, its endothelial cell-autonomous role in acute inflammation remains unclear. Therefore, we examined the role of Ext1 during acute inflammation. In this study, endothelial-specific Ext1-deficient mice (Ext1 and VE-cadherin-Cre) were generated, and their response to endotoxin challenge was investigated using transcriptomics and imaging. Transcriptomic profiling revealed downregulation of heparan sulfate- and glycocalyx-related genes, with upregulation of genes associated with immune activation. Fluorescence imaging demonstrated lectin- and heparan sulfate-defined glycocalyx depletion; dextran extravasation confirmed impaired barrier integrity. Ultrastructural analyses demonstrated a near-complete absence of the luminal glycocalyx at baseline in Ext1-deficient lungs. Following lipopolysaccharide administration, Ext1-deficient mice exhibited altered cytokine kinetics, delayed clearance of neutrophils and CD11b myeloid cells, increased late-phase macrophage accumulation, and prolonged pulmonary edema, indicating impaired resolution of inflammation. Gene set enrichment analysis revealed upregulated leukocyte transendothelial migration, chemokine signaling, and vascular endothelial growth factor pathways, consistent with a persistently activated endothelial phenotype. Endothelial Ext1 is indispensable for heparan sulfate biosynthesis, endothelial glycocalyx integrity, and timely inflammation resolution. Loss of Ext1 leads to an intrinsically pro-inflammatory endothelial state characterized by impaired heparan sulfate-dependent signaling and dysregulated leukocyte-endothelial interactions, heightened vascular permeability, and prolonged tissue injury. Our findings support glycocalyx-targeted therapy in sepsis, acute respiratory distress syndrome, diabetes-associated inflammation, and other conditions of endothelial vulnerability.