Experimental and Therapeutic Medicine实验与治疗医学
Experimental and Therapeutic Medicine(英文缩写 EXP THER MED),ISSN 1792-0981,eISSN 1792-1015,中文译名:实验与治疗医学 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 | 2.751 | Q4 |
| 2022 | 2.700 | Q3 |
| 2023 | 2.400 | Q3 |
| 2024 | 2.300 | Q3 |
| 2025 | 2.200 | Q3 |
Experimental and Therapeutic Medicine 最新收录文献
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1. [Retracted] Hsp70 inducer, 17-allylamino-demethoxygeldanamycin, provides neuroprotection via anti-inflammatory effects in a rat model of traumatic brain injury.
PMID:日期:2026-09-10[This retracts the article DOI: 10.3892/etm.2016.3821.].
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2. Relapsed/refractory multiple myeloma with extramedullary plasmacytomas successfully rechallenged with humanized B-cell maturation antigen-directed chimeric antigen receptor T-cell immunotherapy in an advanced disease stage: A case report.
2. 复发/难治性多发性骨髓瘤伴髓外浆细胞瘤在晚期疾病阶段成功再次接受人源化B细胞成熟抗原靶向嵌合抗原受体T细胞免疫治疗：一例病例报告PMID:日期:2026-09-08Multiple myeloma (MM) is a plasma cell malignancy, and extramedullary plasmacytoma (EMP) is associated with an aggressive biology and poor outcomes. B-cell maturation antigen (BCMA)-directed chimeric antigen receptor T-cell (CAR-T) therapy has shown substantial activity in relapsed/refractory MM (RRMM); however, evidence in patients with EMP, particularly after prior BCMA CAR-T exposure, remains limited. The present study describes the case of a 38-year-old man with RRMM and extensive cranial EMP who progressed after multiple prior therapies, including proteasome inhibitor- and immunomodulatory drug-based regimens, anti-CD38 therapy, carfilzomib-based therapy and a previous non-humanized BCMA CAR-T product. Due to rapidly progressive disease, the patient received bridging cytoreduction followed by fully humanized BCMA CAR-T therapy (equecabtagene autoleucel). After infusion, serum and urine M-protein levels rapidly declined and the craniofacial mass regressed clinically and radiographically. The patient achieved stringent complete response with durable control of extramedullary disease during follow-up. The present case suggests that fully humanized BCMA CAR-T therapy may remain effective in selected patients with RRMM and EMP, even after prior non-humanized BCMA CAR-T failure. These findings support further investigation into retreatment strategies and post-CAR-T maintenance approaches.
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3. Promoting expertise knowledge sharing in paediatric virology: An update (Review).
PMID:日期:2026-09-07Knowledge sharing in medical education is a continuous exchange of skills and expertise between scientists. Paediatric virology is a rapidly developing, new scientific field of medicine, which enhances multidisciplinary, expertise knowledge sharing between paediatric health professionals and scientists of different subspecialties. The present review discusses the recent core topics in paediatric viral infectious diseases discussed during the 11th Workshop on Paediatric Virology organised by the Institute of Paediatric Virology and presents its key messages, including: i) The history of smallpox vaccination; ii) the role of viral co-infections triggering invasive bacterial diseases; iii) the surge of invasive group A streptococcal disease during the post-coronavirus disease 2019 (COVID-19) era; iv) foetal brain imaging findings in maternal severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection; v) the diabetogenic role of Coxsackie viruses in childhood; vi) adenovirus-related central nervous system manifestations in the paediatric population; vii) new challenges and opportunities of hepatis D virus infection in children; viii) the Swedish up-to-date human papillomavirus vaccination experience in childhood.
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4. [Expression of Concern] JWA regulates human esophageal squamous cell carcinoma and human esophageal cells through different mitogen-activated protein kinase signaling pathways.
4. [关注声明] JWA通过不同的丝裂原活化蛋白激酶信号通路调控人食管鳞状细胞癌和人食管细胞PMID:日期:2026-09-07该文献暂无摘要。
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5. {"_":"ACT001 suppresses ox-LDL-mediated macrophage ferroptosis via activating the NRF2 pathway: An mechanistic study relevant to atherosclerosis.","i":["in vitro"]}
5. {"_":"ACT001通过激活NRF2通路抑制ox-LDL介导的巨噬细胞铁死亡：一项与动脉粥样硬化相关的机制研究。","i":["体外实验"]}PMID:日期:2026-09-07Oxidized low-density lipoprotein (ox-LDL) is a key inducer of ferroptosis, which is associated with the progression of atherosclerosis. Macrophages play a notable role in atherosclerosis development, and ferroptosis in these cells contributes to the pathological process of atherosclerosis. However, the potential intervention strategy for ox-LDL-induced RAW264.7 cell ferroptosis remains unclear. ACT001 has emerged as a novel anti-inflammation agent; therefore, experiments were conducted to elucidate the specific effects and mechanism of ACT001 on ox-LDL-induced ferroptosis in RAW264.7 cells. RAW264.7 cells were treated with ox-LDL to establish an ferroptosis model and then co-treated with ACT001. Consequently, the expression of ferroptosis-related markers were evaluated via western blotting, PCR/detection of lipid peroxidation markers (malondialdehyde, glutathione; SOD: Superoxide dismutase; 4-HNE: 4-Hydroxynonenal; lipid reactive oxygen species (ROS) content)/transmission electron microscopy/iron content assay/mitochondrial membrane potential assay and ferrous ion staining. The potential molecular mechanism of ACT001 was further explored by detecting the expression and nuclear translocation of nuclear factor E2-related factor 2 (NRF2) via western blotting, confocal immunofluorescence/CHIP-PCR. Ox-LDL significantly mediated ferroptosis in RAW264.7 cells, as evidenced by increased lipid peroxidation, decreased glutathione content, elevated ROS production and downregulated expression of glutathione peroxidase 4 (GPX4) and solute carrier family 7 member 11 (xCT); however, co-treatment with ACT001 effectively reversed these changes. Mechanistically, ACT001 treatment significantly increased the nuclear translocation of NRF2 and enhanced the enrichment of NRF2 level in the promoter regions of GPX4 and xCT via binding with NRF2, thereby upregulating the expression of GPX4 and xCT. In conclusion, ACT001 effectively ameliorated ox-LDL-triggered ferroptosis in RAW264.7 macrophages through facilitating NRF2 nuclear translocation and upregulating GPX4/xCT expression. The present findings revealed a molecular mechanism linking ACT001 to the inhibition of macrophage ferroptosis, offering preliminary cell-level evidence of the ACT001 therapeutic potential against macrophage-driven pathological events in atherosclerosis.
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6. From mitochondria to innate immunity: The mtDNA-driven cGAS/STING-NLRP3 cascade and its therapeutic implications in neurodegenerative diseases (Review).
6. 从线粒体到天然免疫：mtDNA驱动的cGAS/STING-NLRP3级联反应及其在神经退行性疾病中的治疗意义（综述）PMID:日期:2026-09-04Neurodegenerative diseases (NDDs) are commonly accompanied by persistent low-grade neuroinflammation, yet current therapies rarely achieve durable disease modification. This review aims to systematically delineate the role of mitochondrial DNA (mtDNA) leakage in linking mitochondrial injury to innate immune activation and to explore its pathological significance in NDDs. A comprehensive review of recent literature on mitochondrial stress, mtDNA release and innate immune signaling was conducted. Evidence was integrated regarding the sources of mtDNA immunogenicity, routes of mtDNA escape, mitophagy-lysosome gating mechanisms and the modulation of leakage baseline by aging and metabolic stress. Accumulating evidence indicates that cytosolic mtDNA is sensed by cyclic GMP-AMP synthase (cGAS) and activates the stimulator of interferon (IFN) genes (STING) pathway signaling through the TANK-binding kinase 1 and IFN regulatory factor 3 axis to induce type I IFN responses and promoting NF-κB-driven inflammatory transcription, thereby enhancing NLRP3 inflammasome priming. Oxidized mtDNA, pore-forming membrane events and ionic imbalance further facilitate NLRP3 assembly and pyroptotic execution, exacerbating mitochondrial damage and mtDNA release in a self-amplifying loop. Based on these findings, a modular assessment framework was proposed across the 'input-chronicity-amplification' layers and the potential of mtDNA-cGAS/STING-NLRP3 axis-informed stratified diagnosis and treatment was discussed Central nervous system-targeted delivery, cellular heterogeneity and immune safety windows remain critical for translational research. This review provides a testable mechanistic framework and a clinical evaluation pathway for understanding mtDNA-driven persistent inflammation in NDDs.
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7. Active abdominal compression-decompression cardiopulmonary resuscitation attenuates neuroinflammation associated with TLR4/NF-κB signaling in a rat model of cardiac arrest.
PMID:日期:2026-09-04Cardiac arrest (CA) induces cerebral ischemia-reperfusion injury, which is a major contributor to mortality and neurological dysfunction following resuscitation. Active abdominal compression-decompression cardiopulmonary resuscitation (AACD-CPR) has emerged as a potential alternative to standard cardiopulmonary resuscitation (STD-CPR). The present study aimed to investigate whether AACD-CPR attenuates neuroinflammation after CA/CPR and whether this effect is associated with changes in Toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB)-related signaling. A rat model of CA was established, followed by resuscitation with either STD-CPR or AACD-CPR. Return of spontaneous circulation (ROSC), survival, NDS and neuronal injury were evaluated. The expression levels of TLR4, NF-κB and inflammation-related markers, including tumor necrosis factor-α, interleukin-1 β, glial fibrillary acidic protein (GFAP) and ionized calcium-binding adapter molecule 1 in brain tissue were assessed by western blotting and immunohistochemistry. Compared with STD-CPR, AACD-CPR markedly reduced resuscitation duration and improved early neurological outcomes. Although the ROSC rate and short-term survival rate were numerically higher in the AACD-CPR group than in the STD-CPR group, these differences did not reach statistical significance and therefore should not be interpreted as evidence of a definitive survival benefit. AACD-CPR was also associated with reduced neuronal injury, decreased expression of proinflammatory cytokines and glial activation markers and downregulation of TLR4/NF-κB-related proteins in brain tissue. AACD-CPR improved early neurological outcomes and attenuated neuroinflammatory responses in this rat model of CA/CPR. These effects were accompanied by suppression of TLR4/NF-κB-related signaling. However, as this was a preclinical small-animal study, the findings should be interpreted cautiously and not as evidence that AACD-CPR can clinically replace STD-CPR. Further studies in large-animal models and well-designed clinical investigations are required to validate its safety, feasibility and translational relevance.
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8. Mapping and anatomo-surgical techniques for language preservation in brain tumours (Review).
PMID:日期:2026-09-02Glioma resection surgeries require balance between language functioning protection and maximal tumour removal. Surgical planning is key for the success of resection procedures and the techniques involved are often associated with cortical mapping and tissue differentiation. These techniques include direct electrical stimulation, stereo-electroencephalography, functional magnetic resonance imaging, diffusion tensor imaging, functional ultrasound, hyperspectral imaging and intraoperative optical imaging. The present review explores the anatomical features of language-eloquent areas and the techniques and technologies developed to map cortical areas and distinguish tumour tissue from functional tissue. The benefits and limitations of each technique are discussed, along with their intraoperative and preoperative uses. All techniques are discussed in the context of their effectiveness in the preservation of cortical areas responsible for language processing.
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9. ASF1A: A versatile histone chaperone bridging chromatin dynamics, disease mechanisms and clinical potential (Review).
PMID:日期:2026-09-02Anti-silencing function 1A (ASF1A) is an evolutionarily conserved histone H3/H4 chaperone that mediates nucleosome assembly, DNA replication and DNA damage repair. Beyond these canonical biological functions, aberrant ASF1A expression facilitates disease progression by triggering epigenetic dysregulation in multiple malignant tumors (including leukemia, breast, liver and gastrointestinal cancers) and non-neoplastic disorders (such as atherosclerosis and embryonic developmental defects). Its context-dependent biological effects are mediated via oncogenic signaling cascades and crosstalk between metabolism and epigenetics. Although preclinical studies have validated ASF1A as a promising prognostic biomarker and therapeutic target, relevant clinical trials supporting its clinical application remain absent. This review systematically summarizes the molecular features, pathogenic mechanisms and translational application potential of ASF1A.
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10. Gut microbiome dynamics in acute infectious diarrhea: A conceptual framework from acute dysbiosis toward precision restoration (Review).
PMID:日期:2026-09-02Acute diarrhea affects >1 billion individuals annually, imposing a major health and economic burden worldwide. Although the involvement of the gut microbiota is increasingly acknowledged, the dynamics of microbiota disruption, recovery and related therapeutic opportunities remain poorly integrated. The present review proposed a conceptual framework that synthesizes current understanding of pathogen-driven structural and functional alterations of the microbiota, the staged ecological succession during convalescence (including risks of incomplete restitution) and emerging microbiota-based interventions, ranging from probiotics to phage therapy. The present review further highlighted the potential of artificial-intelligence-driven multi-omics integration, while mapping the distance between current evidence and future precision-medicine goals. Evidence-based interventions were explicitly distinguished from investigational strategies, and microbiota-derived diagnostic biomarkers were discussed as a promising research direction rather than ready-to-deploy clinical tools. Finally, the present review provided evidence-based recommendations to bridge ecological principles with bedside practice, framing acute infectious diarrhea as a severe but often reversible ecological perturbation (an acute dysbiosis) that reveals individual ecological vulnerability and offers a diagnostic window for risk stratification. The present review is intended as a conceptual and evidence-synthesis framework rather than a clinical practice guideline.