EXPERIMENTAL AND MOLECULAR MEDICINE实验与分子医学
EXPERIMENTAL AND MOLECULAR MEDICINE(英文缩写 EXP MOL MED),ISSN 1226-3613,eISSN 2092-6413,中文译名:实验与分子医学 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 | 12.172 | Q1 |
| 2022 | 12.800 | Q1 |
| 2023 | 9.500 | Q1 |
| 2024 | 12.900 | Q1 |
| 2025 | 17.500 | Q1 |
EXPERIMENTAL AND MOLECULAR MEDICINE 最新收录文献
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1. Author Correction: Splenectomy improves liver fibrosis via tumor necrosis factor superfamily 14 (LIGHT) through the JNK/TGF-β1 signaling pathway.
1. 作者更正：脾切除术通过肿瘤坏死因子超家族14（LIGHT）经JNK/TGF-β1信号通路改善肝纤维化PMID:日期:2026-09-25该文献暂无摘要。
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2. {"_":"Breath volatiles reflect diabetic gastroparesis and its recovery by activating Na1.8-expressing neurons in mice.","sub":["v"]}
PMID:日期:2026-09-24Patients with diabetic gastroparesis (DG) experience chronic, challenging symptoms and currently lack effective treatment options. This study examined whether activating Na1.8-expressing neurons could improve gastric motility and whether volatile organic compounds (VOCs) in exhaled breath could serve as non-invasive indicators of disease status and treatment response. In streptozotocin-induced male diabetic mice, chemogenetic activation of Na1.8-expressing neurons improved gastric motility in DG mice. At the same time, breath VOC profiles differed between DG and non-diabetic controls, with diabetic (3 weeks post-induction) and DG (8-12 weeks) mice showing higher 1-butanol levels than the controls. Two VOCs (2,4-dimethyl-1-heptene and 4-methylheptane) formed a potential treatment-response biomarker panel associated with improved gastric emptying, and the classification model achieved an area under the curve of 0.83 in distinguishing stimulated from non-stimulated states. Our data identified Na1.8-expressing neurons as potential modulators of gastric motility and exhaled VOC patterns as exploratory non-invasive markers of disease dynamics, offering a proof-of-concept framework for neuro-modulatory and breath-test-based strategies to monitor and manage gastroparesis.
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3. Author Correction: SET/PP2A signaling regulates macrophage positioning in hypoxic tumor regions by amplifying chemotactic responses.
3. 作者更正：SET/PP2A信号通过放大趋化反应调控巨噬细胞在缺氧肿瘤区域中的定位PMID:日期:2026-09-17该文献暂无摘要。
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4. A refined MASH-HCC model identifies macrophage Gadd45b as a key orchestrator of inflammation-driven neoplastic progression.
PMID:日期:2026-09-16Metabolic dysfunction-associated steatohepatitis (MASH) is emerging as a leading driver of hepatocellular carcinoma (HCC), yet the molecular mechanisms linking metabolic stress, chronic inflammation and tumorigenesis remain poorly understood. Here we established a metabolically relevant, time-efficient MASH-to-HCC model in C57BL/6N mice by combining a MASH diet with controlled CCl administration, enabling stepwise recapitulation of MASH-associated neoplastic progression. Using this model, we identified growth arrest and DNA damage 45b (Gadd45b) as a novel MASH-derived protumorigenic regulator selectively activated under metabolic stress. Integrated analyses of human bulk and single-cell transcriptomic datasets and mouse transcriptomic deconvolution revealed concordant macrophage remodeling and GADD45B/Gadd45b expression dynamics during MASH-to-HCC progression. Mechanistically, fatty acids and TNFα preferentially induced Gadd45b in macrophages, where it amplified TNFα-NF-κB signaling. Macrophage-derived inflammatory signals subsequently induced Gadd45b and NF-κB activation in hepatocytes, establishing a feed-forward inflammatory loop that promoted fibrogenic and partial EMT-like programs and tumor spheroid formation. Importantly, temporal profiling during spheroid formation and progression revealed transient induction of Gadd45b during early spheroid establishment, but not during later progression, indicating that Gadd45b-mediated inflammatory signaling primarily promotes tumor initiation rather than subsequent growth. Consistent with human data, Gadd45b expression increased with disease severity and positively correlated with inflammatory factors in the MASH-HCC model, whereas pharmacological inhibition attenuated the Gadd45b-inflammation signaling axis. Collectively, our findings establish macrophage Gadd45b as a key orchestrator linking metabolic stress, chronic inflammation, and neoplastic transformation during MASH-to-HCC progression. Our refined MASH-HCC model provides a robust platform for mechanistic studies and preclinical evaluation of inflammation-targeted therapies.
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5. {"_":"FAP pericyte-like cells promote monocyte differentiation into tumor-associated macrophages in glioblastoma.","sup":["+"]}
5. 胶质母细胞瘤中，FAP阳性的血管周细胞样细胞促进单核细胞分化为肿瘤相关巨噬细胞。["+"]PMID:日期:2026-09-11Glioblastoma (GBM) is a highly aggressive primary brain tumor characterized by profound immunosuppression that facilitates tumor progression and promotes therapeutic resistance. Fibroblast activation protein (FAP), a recognized theranostic target in multiple cancers, is upregulated in GBM and predominantly expressed by pericyte-like stromal cells. Here we identify a role for FAP⁺ pericyte-like cells in shaping the GBM immune microenvironment through monocyte recruitment and differentiation. Analysis of The Cancer Genome Atlas (TCGA) datasets, supported by reverse-transcription quantitative PCR and immunohistochemistry, revealed that elevated FAP expression-serving as a proxy for the abundance of FAP⁺ pericyte-like cells-is associated with an immune-enriched tumor microenvironment characterized by higher macrophage abundance and elevated expression of M2 polarization markers. Spatial analyses, including immunofluorescence and spatial transcriptomics, demonstrated that immunosuppressive macrophages preferentially localize in proximity to FAP⁺ pericytes. Single-cell RNA sequencing identified these FAP⁺ cells as a distinct perivascular stromal subset with a unique expression pattern of extracellular matrix components and cytokines, including CCL2 and CSF1, with corresponding receptors expressed on myeloid cells. Functional assays using patient-derived FAP⁺ pericyte-like cells confirmed their ability to attract monocytes via soluble mediators and to promote their differentiation and polarization into tumor-associated macrophages with immunoregulatory features, partly mediated by the CSF1-CSF1R axis. Orthotopic co-implantation experiments in mice further supported their capacity to enhance myeloid infiltration in vivo. Consistent with these biological effects, a transcriptional signature characteristic of FAP⁺ pericytes correlated with worse overall survival in patients with GBM. Together, these findings position FAP⁺ pericyte-like cells as modulators of the GBM immune landscape, fostering a tumor-permissive niche by promoting the differentiation of circulating monocytes into immunoregulatory macrophages. Targeting this stromal population may offer new therapeutic avenues to reprogram tumor-associated immune responses in GBM.
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6. TRANsCre-DIONE transdifferentiates scar-forming reactive astrocytes into functional motor neurons.
6. TRANsCre-DIONE 将形成瘢痕的反应性星形胶质细胞转分化为功能性运动神经元PMID:日期:2026-09-11In spinal cord injury (SCI), the scar-forming reactive astrocytes with upregulated glial fibrillary acidic protein (GFAP) proliferate aberrantly near the injury site, representing a potential cellular source for transdifferentiation into neurons to replenish dead neurons. However, the conventional use of GFAP promoter to target reactive astrocytes has two inherent problems: inadvertent conversion of normal astrocytes and low efficiency due to progressive weakening of promoter activity during transdifferentiation. Here, we present TRANsCre-DIONE, a dual-promoter split-Cre system combining GFAP and Lcn2 regulatory elements with Cre-dependent Neurog2 expression under the EF1α promoter, enabling selective targeting of scar-forming reactive astrocytes. This approach achieved 87% conversion efficiency and 96% specificity in vivo. After SCI, TRANsCre-DIONE caused transdifferentiation into Isl1-positive and ChAT-positive motor neurons, reduced astrogliosis, enhanced regeneration in surrounding cells, and a significant motor recovery. These findings suggest that TRANsCre-DIONE enables efficient and selective astrocyte-to-neuron conversion and represents a promising strategy for SCI repair.
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7. Pharmacological modulation of GPR84 revealed by dual states structures and immune functional assays.
PMID:日期:2026-09-10G-protein-coupled receptor 84 (GPR84) is an orphan class A GPCR selectively activated by medium chain fatty acids and highly expressed in immune cells, where it modulates pro-inflammatory signaling. The structural basis of GPR84 inactivation and antagonism has remained unclear, limiting the rational design of pathway-selective modulators despite its clinical relevance in metabolic inflammation and fibrotic diseases. Here, we report cryo-electron microscopy structures of human GPR84 in inactive and active states. The 3.5 Å inactive structure bound to the antagonist GLPG1205 reveals a lid-like conformation of extracellular loop 2 and an inward reorientation of Arg172, with the antagonist head group blocking the allosteric sodium-binding site. Molecular dynamics simulations further support these findings, identifying an aberrant TM5, TM6 lateral entry gate. By contrast, the 3.17 Å agonist ZQ-16, Gαi complex, shows a rearranged toggle switch and comparative analyses highlight extracellular loop 2 conformational plasticity. Immune functional assays in THP-1 cells demonstrated that ZQ-16 elicited GPR84-dependent activation and cytokine production, which were effectively abrogated by GLPG1205. Mutagenesis combined with functional assays validates key ligand interactions, providing a framework for the rational design of pathway selective GPR84 modulators.
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8. Deficiency of protein kinase Cδ reprograms macrophage immunometabolism to suppress pyroptosis and stabilize atherosclerotic plaques.
8. 蛋白激酶Cδ的缺乏重编程巨噬细胞免疫代谢，从而抑制细胞焦亡并稳定动脉粥样硬化斑块PMID:日期:2026-09-10While atherosclerotic plaque vulnerability drives acute coronary syndrome, the regulatory mechanisms underlying plaque stability remain unclear. Protein kinase Cδ (PKCδ) has been implicated in atherosclerosis progression, but its specific role in plaque vulnerability and the underlying mechanisms require clarification. We analyzed PKCδ expression in human atheroma datas and investigated its role using low-density lipoprotein receptor-knockout mice with global and myeloid-specific PKCδ deletion. Plaque morphology, necrotic core formation, and fibrous cap thickness were evaluated. Macrophage metabolic profiling, mitochondrial function, inflammatory responses, and pyroptosis markers were assessed using biochemical and molecular approaches. Human atheroma analysis revealed elevated PKCδ expression, particularly in macrophages within ruptured plaques. PKCδ deletion in mice reduced necrotic core formation and increased fibrous cap thickness in both global and myeloid-specific models. Mechanistically, macrophage PKCδ deficiency improved mitochondrial fitness by promoting mitochondrial oxidative phosphorylation and elevating α-ketoglutarate (α-KG) levels. This metabolic shift reduced pro-inflammatory responses through PIK3AP1-mTORC2 activation and downregulated NLRP3 inflammasome-mediated pyroptosis. Dimethyl α-ketoglutarate (DKG) supplementation provided similar protective effects. Both human and in vivo analyses revealed PKCδ association with pyroptosis markers, including NLRP3, caspase-1, IL-1β, and GSDMD, whereas PKCδ deficiency reduced their co-localization with CD68⁺ macrophages. In conclusion, PKCδ serves as a key regulator of macrophage inflammation, pyroptosis, and mitochondrial dysfunction in atherosclerotic plaques. PKCδ deficiency promotes metabolic reprogramming that stabilizes plaques through reduced pyroptosis and enhanced mitochondrial function. These findings highlight PKCδ as a potential therapeutic target to reduce acute cardiovascular events by modulating plaque stability.
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9. Linking visceral fat accumulation to gut microbiota: key bacterial taxa and their roles in the glycogen synthesis pathway.
PMID:日期:2026-09-10Obesity, marked by visceral fat accumulation, has a complex relationship with the gut microbiome that impacts body weight and fat accumulation. However, previous studies did not account for fat distribution, reflecting only overall fat mass, leaving specifics of this relationship partially understood. Here we analyzed the mechanistic links between visceral fat and the microbiome in a large cohort of healthy Koreans. Using permutational multivariate analysis of variance and prediction modeling, we examined associations between microbial profiles and metabolic variables including insulin, triglycerides, waist circumference and visceral fat. The strongest correlations were noted with specific enterotypes. Shotgun sequencing revealed that visceral fat is linked to the glycogen synthesis pathway influenced by Dorea longicatena and Bifidobacterium adolescentis. This suggests that these specific microbial signatures and their associated functional potential play a role in visceral fat-related obesity. To validate these findings, we conducted an in vivo study using diet-induced obesity mouse model. Oral administration of D. longicatena or B. adolescentis significantly promoted body weight gain and fat mass expansion and induced hepatic lipogenic gene upregulation. The prevalence of these strains in Korean and American populations highlights their global relevance, contributing to the development of personalized treatments and advanced health strategies.
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10. SMRT regulation of nuclear receptors orchestrates bile acid homeostasis.
10. 核受体的SMRT调控协调胆汁酸稳态PMID:日期:2026-09-09Nuclear receptors are key effectors of metabolic programs; however, the contribution of co-regulatory complexes in maintaining metabolic homeostasis is not fully understood. Here, we show that modulation of the constitutive androstane receptor (CAR) by the co-repressor silencing mediator of retinoic acid and thyroid hormone receptors (SMRT) is required for bile acid (BA) homeostasis. Transcriptional changes in the livers of mice harboring a targeted disruption in one of the nuclear receptor-interacting domains (RIDs), SMRT mice, revealed increased expression of CAR target genes involved in BA export. Consistent with this, SMRT mice challenged with a high-fat diet showed increased BAs in serum and urine with commensurate decreases in the liver and intestines. Notably, the reduction in intestinal BAs led to decreased activity of the BA receptor farnesoid X receptor (FXR). This reduction in FXR activity compromised the integrity of the intestinal barrier, increased bacterial burden, and augmented intestinal inflammation. Moreover, SMRT mice were susceptible to intestinal damage, with higher mortality rates in acute colitis and colitis-associated cancer models. Treatment with a synthetic FXR agonist (XL335) rescued SMRT mice during acute colitis. Collectively, these studies highlight the importance of SMRT in maintaining BA homeostasis through direct and indirect regulation of hepatic CAR and intestinal FXR activity, respectively, and point to potential therapeutic routes for combating intestinal pathologies associated with a high-fat diet.