The Kaohsiung journal of medical sciences最新文献_第9页

Interactive Roles of Metabolic Dysfunction-Associated Steatotic Liver Disease and Nutritional Status in the Prognosis of Patients With Hepatocellular Carcinoma After Surgical Resection. 代谢功能障碍相关脂肪变性肝病和营养状况在肝细胞癌术后预后中的相互作用

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-03 DOI: 10.1002/kjm2.70256

Chun-Ting Ho, Chien-An Liu, Chia-Jung Ho, Yi-Chen Lin, Shin-Yu Tsai, Hao-Jan Lei, Shu-Cheng Chou, Yi-Hsiang Huang, Ming-Chih Hou, Jaw-Ching Wu, Chien-Wei Su

{"title":"Interactive Roles of Metabolic Dysfunction-Associated Steatotic Liver Disease and Nutritional Status in the Prognosis of Patients With Hepatocellular Carcinoma After Surgical Resection.","authors":"Chun-Ting Ho, Chien-An Liu, Chia-Jung Ho, Yi-Chen Lin, Shin-Yu Tsai, Hao-Jan Lei, Shu-Cheng Chou, Yi-Hsiang Huang, Ming-Chih Hou, Jaw-Ching Wu, Chien-Wei Su","doi":"10.1002/kjm2.70256","DOIUrl":"10.1002/kjm2.70256","url":null,"abstract":"The prognostic effect of concurrent metabolic dysfunction-associated steatotic liver disease (MASLD) on outcomes for hepatocellular carcinoma (HCC) patients remains unclear. The Prognostic Nutritional Index (PNI) reflects nutritional and inflammatory status and is a well-known prognostic factor. We therefore aimed to evaluate and compare the prognostic role of PNI in patients with HCC with and without concurrent MASLD undergoing curative surgical resection. In our retrospective study, 991 patients undergoing curative HCC resection were stratified according to MASLD status and pre-operative PNI (cut-off: 45). Overall survival (OS) and recurrence-free survival (RFS) were analyzed using Kaplan-Meier methods and Cox proportional hazards models. Further subgroup analysis was performed according to their concurrent viral hepatitis status. High PNI was identified as an independent protective factor against poor OS for the entire cohort (hazard ratio [HR]: 0.65; 95% confidence interval [CI]: 0.49-0.87, p = 0.004). The Kaplan-Meier analysis showed that the high-PNI/MASLD group had the best OS, while the low-PNI/no-MASLD group had the worst. Subgroup analysis indicated that high PNI was an independent protective factor for OS only in the no-MASLD group (HR: 0.59, p = 0.003) but not the MASLD group (HR: 0.94, p = 0.793). Its prognostic effect was more significant in HCC patients without concurrent MASLD or with chronic hepatitis B. To conclude, a better nutritional status, assessed by PNI, is a valuable prognostic marker for patients with HCC. Its protective effect on OS is significantly pronounced in patients without concurrent MASLD, indicating that MASLD status modifies the prognostic utility of PNI.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70256"},"PeriodicalIF":3.1,"publicationDate":"2026-07-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13399853/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148383453","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

PDCD5 Contributes to Airway Epithelial Cell Damage via Mitochondrial Pathway and Participates in COPD Pathogenesis. PDCD5通过线粒体途径参与气道上皮细胞损伤并参与COPD发病机制

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2025-12-25 DOI: 10.1002/kjm2.70165

Hu Shan, Rui Zhang, Yu-Er Li, Rui Li, Shao-Bo Ge, Jin Liu, Shi-Yuan Yao, Xia Yang, Tao Zhang, Ming Zhang

{"title":"PDCD5 Contributes to Airway Epithelial Cell Damage via Mitochondrial Pathway and Participates in COPD Pathogenesis.","authors":"Hu Shan, Rui Zhang, Yu-Er Li, Rui Li, Shao-Bo Ge, Jin Liu, Shi-Yuan Yao, Xia Yang, Tao Zhang, Ming Zhang","doi":"10.1002/kjm2.70165","DOIUrl":"10.1002/kjm2.70165","url":null,"abstract":"Airway epithelial injury plays a critical role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Mitochondrial dysfunction is implicated in this injury, while the underlying mechanism remains incompletely understood. RNA sequencing was conducted to identify key genes involved in mitochondrial dysfunction in airway epithelial injury induced by cigarette smoke extract (CSE). We identified 1981 significantly up-regulated and 4952 down-regulated differentially expressed genes (DEGs) in CSE-treated airway epithelial cells. A protein-protein interaction network constructed from the DEGs revealed that several key genes were involved in CSE-induced airway epithelial injury. Additionally, PDCD5 was identified as a hub gene potentially linked to mitochondrial dysfunction. PDCD5 expression was significantly increased in the airway epithelium of COPD patients and the corresponding experimental mice. The mRNA and protein expression levels of PDCD5 were significantly increased in concentration- and time-dependent manners in airway epithelial cells treated with CSE. PDCD5 silencing significantly attenuated CSE-induced mitochondrial reactive oxygen species (ROS) accumulation, mitochondrial membrane potential loss, and intracellular ATP depletion. Transmission electron microscopy revealed that PDCD5 siRNA treatment ameliorated CSE-induced mitochondrial structural damage. Moreover, PDCD5 knockdown significantly reduced intracellular ROS accumulation, attenuated apoptosis increases, and inhibited cell viability decline in airway epithelial cells treated with CSE. Our findings demonstrate that PDCD5 contributes to airway epithelial cell damage through the mitochondrial pathway and participates in the pathogenesis of COPD, implicating it as a potential diagnostic biomarker and therapeutic target for COPD.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70165"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344223/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145828768","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Fat Mass and Obesity-Associated Protein Contributes to Tumorigenesis and Drug Resistance of Diffuse Large B-Cell Lymphoma by Suppressing N6-Methyladenosine Methylation of Myc. 脂肪量和肥胖相关蛋白通过抑制Myc的n6 -甲基腺苷甲基化参与弥漫性大b细胞淋巴瘤的肿瘤发生和耐药

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2026-01-13 DOI: 10.1002/kjm2.70158

Ting-Ting Lu, Jin-Hao Chen, Yan-Fang Wang, Xiao Wu, Hui-Yun Ni, Qiu-Rong Zhang

{"title":"Fat Mass and Obesity-Associated Protein Contributes to Tumorigenesis and Drug Resistance of Diffuse Large B-Cell Lymphoma by Suppressing N6-Methyladenosine Methylation of Myc.","authors":"Ting-Ting Lu, Jin-Hao Chen, Yan-Fang Wang, Xiao Wu, Hui-Yun Ni, Qiu-Rong Zhang","doi":"10.1002/kjm2.70158","DOIUrl":"10.1002/kjm2.70158","url":null,"abstract":"Ibrutinib resistance remains a major obstacle in the treatment of diffuse large B-cell lymphoma (DLBCL). Fat mass and obesity-associated protein (FTO) has been implicated in drug resistance through its regulation of N6-methyladenosine (m6A) modifications; however, whether FTO mediates ibrutinib resistance in DLBCL remains unclear. In this study, we found that FTO expression was significantly upregulated in patient samples and DLBCL cell lines. Functional assays showed that FTO knockout or knockdown suppressed cell proliferation and colony formation, whereas FTO overexpression promoted tumor growth and increased ibrutinib half-maximal inhibitory concentration. Mechanistically, FTO directly bound to myelocytomatosis oncogene (Myc) mRNA and removed m6A modifications, stabilizing Myc transcripts and enhancing Myc protein expression. Methylated RNA immunoprecipitation-quantitative polymerase chain reaction confirmed that FTO knockout increased m6A enrichment on Myc mRNA, leading to decreased Myc stability. Rescue experiments showed that reintroducing Myc partially restored the proliferative and drug-resistant phenotype of FTO-deficient cells. Consistently, in xenograft models, FTO promoted tumor growth and ibrutinib resistance in a manner partly dependent on Myc. Overall, FTO promotes DLBCL progression and ibrutinib resistance by demethylating Myc mRNA and stabilizing its expression. These findings highlight the FTO-m6A-Myc axis as a potential therapeutic target for overcoming drug resistance in DLBCL.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70158"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Lysosome Evanescence Mediates Autophagic Flux Impairment in Glucose Imbalanced Environments. 葡萄糖不平衡环境中溶酶体消失介导自噬通量损伤。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2025-12-13 DOI: 10.1002/kjm2.70145

Yuan-Chen Cheng, Ling-Li Chang, Hung-Chen Wang, Wei-Chun Hung, Chia-Hua Hsieh, Yi-Hsuan Wang, Kuang-I Cheng

{"title":"Lysosome Evanescence Mediates Autophagic Flux Impairment in Glucose Imbalanced Environments.","authors":"Yuan-Chen Cheng, Ling-Li Chang, Hung-Chen Wang, Wei-Chun Hung, Chia-Hua Hsieh, Yi-Hsuan Wang, Kuang-I Cheng","doi":"10.1002/kjm2.70145","DOIUrl":"10.1002/kjm2.70145","url":null,"abstract":"Schwann cells (SCs) support axonal function and promote nerve regeneration. This study investigated how various glucose concentrations influence SC viability, oxidative stress, and autophagy, which contribute to diabetic neuropathy. RSC96 SCs were cultured under five glucose conditions (0, 2.5, 5.5, 50, or 100 mM) for 24, 48, and 72 h. Cell viability was assessed by MTT; ROS levels were determined by DCFDA staining, and apoptosis and ER stress markers, as well as autophagy-related proteins were assessed by Western blotting. Autophagic flux was also analyzed using bafilomycin A1 and Cyto-ID. The results revealed time-dependent increases in cell death across all glucose conditions, especially under deprivation and low glucose (LG) conditions. ROS, CHOP, Bax, and cleaved caspase-3 levels increased from 24 to 72 h. The initial increase in the LC3B-II/I ratio indicated that autophagy was overactivated under glucose deprivation or LG conditions but impaired by 72 h, as indicated by reduced Lamp-2 expression. High glucose conditions led to early and persistent autophagy suppression, with minimal autophagic flux and vacuole formation. These findings demonstrate that SCs are sensitive to glucose levels and undergo distinct autophagic impairments through different mechanisms under persistent low or high glucose environments.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70145"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344340/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145752395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular Mechanism of the IRF1/NFE2L1-DT/ALKBH5/Cx43 Axis in Radiation-Induced Injury in Vascular Endothelial Cells Through Pyroptosis. IRF1/NFE2L1-DT/ALKBH5/Cx43轴通过热亡参与辐射诱导血管内皮细胞损伤的分子机制

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2025-12-24 DOI: 10.1002/kjm2.70159

Chen Li, Jia-Wen Yang, Yong-Rui Jia, Jie Zhang, Qiao Gou

{"title":"Molecular Mechanism of the IRF1/NFE2L1-DT/ALKBH5/Cx43 Axis in Radiation-Induced Injury in Vascular Endothelial Cells Through Pyroptosis.","authors":"Chen Li, Jia-Wen Yang, Yong-Rui Jia, Jie Zhang, Qiao Gou","doi":"10.1002/kjm2.70159","DOIUrl":"10.1002/kjm2.70159","url":null,"abstract":"Radiotherapy effectively eradicates tumor cells but can also trigger pyroptotic damage in vascular endothelial cells. This study investigates the role of interferon regulatory factor 1 (IRF1) in radiation-induced endothelial injury, aiming to provide mechanistic insights for optimizing radiotherapy. Human umbilical vein endothelial cells (HUVECs) were exposed to x-ray irradiation, after which cell viability, lactate dehydrogenase (LDH) release, γ-H2AX foci formation, and the expression of pyroptosis-associated proteins (NLRP3, Cleaved Caspase-1, GSDMD-N, IL-1β, IL-18) were assessed. Expression levels of IRF1, NFE2L1-DT, PELP1, ALKBH5, and Cx43 were quantified. Chromatin enrichment of IRF1 at the NFE2L1-DT promoter and IRF1-NFE2L1-DT interactions were examined, along with NFE2L1-DT or ALKBH5 binding to PELP1. The enrichment of m6A modifications on Cx43 transcripts was also evaluated. X-ray exposure reduced HUVEC viability, elevated LDH release, increased γ-H2AX foci, and upregulated IRF1, along with pyroptosis markers. Silencing IRF1 reversed these changes. Mechanistically, IRF1 directly bound to and increased NFE2L1-DT expression. NFE2L1-DT interacted with PELP1 to enhance the binding of PELP1 to and ALKBH5 mRNA, thus upregulating ALKBH5 expression. ALKBH5-mediated m6A demethylation subsequently downregulated Cx43 expression. Overexpression of NFE2L1-DT or ALKBH5, or silencing Cx43, attenuated the protective effects of IRF1 silencing against radiation-induced damage. These findings indicate that radiation-induced IRF1 upregulation leads to endothelial injury by promoting pyroptosis through the NFE2L1-DT/ALKBH5/Cx43 axis.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70159"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145822512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Exome Sequencing Identifies Variants in MLH1 and ERBB2 as Potential Cancer-Predisposing Factors in Familial Early-Onset Colorectal Cancer. 外显子组测序鉴定MLH1和ERBB2变异是家族性早发性结直肠癌的潜在癌症易感因素。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2026-01-02 DOI: 10.1002/kjm2.70166

Behnaz Bagheri, Neda Mohsen-Pour, Najmeh Salehi, Pardis Ketabi Moghadam, Adel Zeinalpour, Amir Sadeghi, Samira Kalayinia, Nayeralsadat Fatemi

{"title":"Exome Sequencing Identifies Variants in MLH1 and ERBB2 as Potential Cancer-Predisposing Factors in Familial Early-Onset Colorectal Cancer.","authors":"Behnaz Bagheri, Neda Mohsen-Pour, Najmeh Salehi, Pardis Ketabi Moghadam, Adel Zeinalpour, Amir Sadeghi, Samira Kalayinia, Nayeralsadat Fatemi","doi":"10.1002/kjm2.70166","DOIUrl":"10.1002/kjm2.70166","url":null,"abstract":"Colorectal cancer (CRC) has raised considerable health concerns worldwide, with increasing incidence rates, specifically among younger populations. Despite remarkable progress in diagnosing and treating various diseases, the genetic basis of CRC remains only partially understood. This paper aims to examine novel genetic variants associated with CRC in Iranian patients. We performed whole-exome sequencing (WES) in two Iranian families with a history of early-onset CRC. Candidate variants were validated by Sanger sequencing and assessed for segregation. Pathogenicity was evaluated through comprehensive in silico analysis and the application of ACMG/AMP guidelines. Analysis revealed two clinically significant variants. In Family 1, we identified a heterozygous stop-gain variant in MLH1 (c.1043T>A, p.Leu348), a known pathogenic mutation consistent with Lynch syndrome. In Family 2, we discovered a previously undocumented heterozygous missense variant in ERBB2 (c.2268G>T, p.Arg756Ser). Through a detailed ACMG assessment, this ERBB2 variant was classified as Likely Pathogenic based on its location in a critical tyrosine kinase domain, absence from population databases, and concordant deleterious in silico predictions. WES offers a deeper understanding of CRC genetics, suggesting potential biomarkers with promising applications for early diagnosis and targeted treatments, eventually improving patient-related outcomes. The results of this study underscore the significant contribution of genetic screening to the well-being of high-risk families and offer valuable insights for targeted therapeutic approaches.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70166"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Association Between Body Mass Index and Depression/Anxiety in an East Asian Population: A Mendelian Randomization Study. 东亚人群体重指数与抑郁/焦虑之间的关系：一项孟德尔随机研究

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2025-12-24 DOI: 10.1002/kjm2.70161

Perl Han Lee, Szu-Chia Chen, Chien-Hung Lee, Jiun-Hung Geng, Chih-Hung Ko

{"title":"Association Between Body Mass Index and Depression/Anxiety in an East Asian Population: A Mendelian Randomization Study.","authors":"Perl Han Lee, Szu-Chia Chen, Chien-Hung Lee, Jiun-Hung Geng, Chih-Hung Ko","doi":"10.1002/kjm2.70161","DOIUrl":"10.1002/kjm2.70161","url":null,"abstract":"Obesity and psychiatric disorders are the leading causes of global morbidity. Epidemiological studies suggest a bidirectional link between higher body mass index (BMI) and mental health outcomes, but the direction of causality remains uncertain due to confounding and reverse causation. We performed a Mendelian randomization (MR) analysis using genetic instruments for BMI (13 and 17 single-nucleotide polymorphisms [SNPs] identified in the Taiwan Biobank) from 107,191 Taiwanese adults (4855 \"cases\" with depression or anxiety and 102,336 \"controls\") to examine the association between BMI and depression and anxiety symptoms. The primary MR results revealed an inverse causal association between the two. An inverse-variance weighted analysis using 17 SNPs indicated that each one-unit increase in genetically predicted BMI was associated with a lower risk of depression and anxiety symptoms. Analyses restricted to 13 strong BMI-associated SNPs revealed a similar inverse direction of effect. The results suggest that higher BMI may be associated with a reduced risk of psychiatric disorders in this East Asian population, highlighting potential differences by population or underlying mechanism. These findings demonstrate how MR can clarify complex exposure-outcome relationships and highlight the need to explore the biological and psychosocial pathways connecting adiposity and mental health.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70161"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344266/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145822429","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Enriched Environment Enhances Motor Function in Mice With Cerebral Infarction by Promoting mTOR-Dependent Autophagy in the Contralateral Dentate Nucleus. 富集环境通过促进对侧齿状核mtor依赖性自噬增强脑梗死小鼠运动功能。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2026-01-05 DOI: 10.1002/kjm2.70167

Chuan-Jie Wang, Ke-Wei Yu, Jun-Fa Wu, Feng Tao

{"title":"Enriched Environment Enhances Motor Function in Mice With Cerebral Infarction by Promoting mTOR-Dependent Autophagy in the Contralateral Dentate Nucleus.","authors":"Chuan-Jie Wang, Ke-Wei Yu, Jun-Fa Wu, Feng Tao","doi":"10.1002/kjm2.70167","DOIUrl":"10.1002/kjm2.70167","url":null,"abstract":"Although environmental enrichment (EE) promotes post-stroke motor recovery, the mechanisms underlying its regulation of cerebellar dentate nucleus (DN) plasticity remain unclear; this study therefore investigated how EE coordinates autophagy, mitochondrial homeostasis, and synaptic remodeling in the contralateral DN to facilitate functional restoration. Using a permanent middle cerebral artery occlusion (pMCAO) mouse model, we combined behavioral tests (rotarod and ladder rung) with electron microscopy, Western blotting (LC3B, p62, mTOR/p-mTOR), and ELISA (TNF-α, IL-1β, IL-6) to assess motor function, ultrastructural changes, autophagy, and neuroinflammation. Results demonstrated that EE significantly improved cerebellar-mediated motor coordination, reduced neuronal degeneration, and preserved mitochondrial integrity, while enhancing autophagic activity via increased LC3B expression and decreased p62 accumulation. Ultrastructural analysis revealed elevated synaptic density and a shift toward mitochondrial rejuvenation, paralleled by attenuated neuroinflammatory responses and suppressed pro-inflammatory cytokine levels, consistent with mTOR pathway inhibition. These findings indicate that EE promotes motor recovery by activating a self-reinforcing repair loop in the DN, wherein autophagy-mediated mitochondrial clearance and neuroinflammation suppression create a permissive microenvironment for synaptic remodeling, thereby establishing the DN as a pivotal hub for EE's therapeutic effects and supporting combinatory strategies targeting autophagy-mitochondrial pathways to optimize rehabilitation.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70167"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145902052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction to "Prognostic Factors Impacting Surgical Resection Outcomes in Elderly Patients With Brain Metastasis". 更正“影响老年脑转移患者手术切除结果的预后因素”。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2026-06-07 DOI: 10.1002/kjm2.70246

引用次数: 0

Matrine Attenuates Neurological Deficits and Neuroinflammation by Inhibiting the HMGB1/RAGE Axis and Ferroptosis in Intracerebral Hemorrhage Mice. 苦参碱通过抑制脑出血小鼠HMGB1/RAGE轴和铁下沉减轻神经功能缺损和神经炎症。

IF 3.1

The Kaohsiung journal of medical sciences Pub Date : 2026-07-01 Epub Date: 2025-12-16 DOI: 10.1002/kjm2.70157

Pan-Di Chen, Tao-Tao Shi, Dan-Yang Hu, Xiao-Na Su, Jian-Xiang Jin, Mao-Song Chen, Hao Wang, Wei Chen

{"title":"Matrine Attenuates Neurological Deficits and Neuroinflammation by Inhibiting the HMGB1/RAGE Axis and Ferroptosis in Intracerebral Hemorrhage Mice.","authors":"Pan-Di Chen, Tao-Tao Shi, Dan-Yang Hu, Xiao-Na Su, Jian-Xiang Jin, Mao-Song Chen, Hao Wang, Wei Chen","doi":"10.1002/kjm2.70157","DOIUrl":"10.1002/kjm2.70157","url":null,"abstract":"Intracerebral hemorrhage (ICH) is a life-threatening stroke subtype that lacks effective drug therapy. In the context of ICH, neuroinflammation, and ferroptosis are key contributors to secondary brain injury. In this study, we assessed the neuroprotective effects of matrine (MAT) and its mechanism of action involving the HMGB1/RAGE axis in an ICH mouse model. ICH was induced in mice by autologous blood injection. MAT (1.5 or 20 mg/kg) was administered orally 5 min postinduction. ICH significantly upregulated RAGE and its associated proteins (HMGB1, protein kinase C [PKC], phospholipase C [PLC], and β-amyloid), confirming pathway activation. Molecular docking revealed a specific hydrogen bond interaction between MAT and RAGE but not with PKC or PLC. MAT improved neurological performance, reduced hematoma volume and brain edema, and restored blood-brain barrier integrity through upregulation of tight junction proteins (ZO-1, Occludin, Claudin-4). MAT suppressed activation of the HMGB1/RAGE pathway and downstream kinases JNK, p38, ERK1/2, and NF-κB p65. It also decreased IL-1β, IL-6, and TNF-α levels, reduced Bax, increased Bcl-2, and mitigated neuronal apoptosis. Additionally, MAT lowered Fe2+ accumulation, inhibited ACSL4, and restored GPX4 levels, indicating ferroptosis suppression. RAGE knockdown mimicked the effects of MAT and negated its therapeutic benefits. MAT induced no detectable liver or kidney toxicity. This study is the first to demonstrate that MAT alleviates ICH-induced neurological deficits by targeting the HMGB1/RAGE axis-mediated ferroptosis, thereby extending the current understanding of the neuroprotective mechanisms of MAT beyond its known anti-inflammatory and antioxidant actions.","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70157"},"PeriodicalIF":3.1,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13344244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145764723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0