The Kaohsiung journal of medical sciences最新文献

{"title":"Acute Effects of the 5-Hydroxytryptamine Type 4 Receptor Agonist Mosapride on Pharyngeal Swallowing Physiology in Adults.","authors":"Shu-Wei Liang, Jui-Sheng Hung, Taher Omari, Ming-Wun Wong, Wei-Yi Lei, Tso-Tsai Liu, Chih-Hsun Yi, Chien-Lin Chen","doi":"10.1002/kjm2.70125","DOIUrl":"https://doi.org/10.1002/kjm2.70125","url":null,"abstract":"<p><p>The 5-hydroxytryptamine type 4 receptor agonist mosapride is known to modulate esophageal peristalsis and enhance lower esophageal sphincter compliance. However, its impact on oropharyngeal swallowing physiology remains insufficiently characterized. This study aimed to investigate the acute effects of mosapride on oropharyngeal swallowing dynamics in adults. Participants received either oral mosapride (40 mg) or placebo 1 h prior to testing in a randomized, crossover design. High-resolution impedance manometry was performed using a solid-state catheter to measure pressure and impedance within the oropharyngeal segment. Each participant underwent at least three swallows of 5, 10, and 20 mL thin and thick liquids administered by syringe. Manometric data were analyzed using the Swallow Gateway web-based platform. Twenty-four volunteers (13 male, mean age, 33 years; range, 24-56 years) completed the study. During thick swallows, mosapride significantly increased upper esophageal sphincter (UES) maximal opening admittance compared to placebo (5 mL: p = 0.017; 10 mL: p = 0.008) and reduced UES integrated relaxation pressure (10 mL: p = 0.018; 20 mL: p = 0.017). No significant effects were observed during thin liquid swallows. A marginal reduction in pre-deglutitive UES basal pressure was noted during 5 mL thick swallows (p = 0.050). Following adjustment using repeated measures ANOVA, only the reduction in UES basal pressure remained statistically significant (p = 0.040). Acute administration of oral mosapride results in reduced UES basal tone in adults. These findings provide novel physiological evidence suggesting that mosapride may modulate neuroregulatory mechanisms controlling UES contractility.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70125"},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260516","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Denosumab Adherence on Renal Function and Mortality Rates in Type 2 Diabetes Patients With Osteoporosis.","authors":"Yu-Chuan Chang, Jian-Chih Chen, Sung-Yen Lin, Kun-Der Lin, Pei-Shan Ho, Chung-Hwan Chen, Yin-Chih Fu, Tien-Ching Lee","doi":"10.1002/kjm2.70124","DOIUrl":"https://doi.org/10.1002/kjm2.70124","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM) is associated with an increased risk of osteoporosis and fractures, and denosumab, a non-kidney-excreted antiresorptive medication, represents a viable alternative to bisphosphonates for osteoporosis treatment in patients with T2DM. This study aimed to investigate the association among denosumab adherence, renal function, and all-cause mortality in patients with T2DM and osteoporosis. New denosumab users between 2010 and 2017 were identified from an electronic health record database, and after exclusion, 536 participants were screened and analyzed based on their 2-year drug adherence: high adherence (HA) defined as three or four doses, and low adherence (LA) defined as one or two doses. The 1-year average estimated glomerular filtration rate (eGFR) was calculated, and all-cause mortality was analyzed using Kaplan-Meier curves and Cox regression models. The study included 286 and 250 subjects in the HA and LA groups, respectively, and although eGFR declined in both groups, renal function remained comparable between the groups. The all-cause mortality rate was significantly lower in the HA group compared to the LA group (adjusted hazard ratio: 0.52, 95% confidence interval: 0.29-0.92). High denosumab adherence was found to be associated with a lower risk of all-cause mortality among patients with T2DM and osteoporosis without significantly impacting renal function, highlighting the potential benefits of maintaining regular denosumab treatment in this high-risk population. Nevertheless, this observational study design indicates association rather than causation, and further prospective research is warranted to validate these results and elucidate the mechanisms underlying the relationships observed in this study.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70124"},"PeriodicalIF":3.1,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145260543","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Kaempferitrin's Dual Assault: Inducing Apoptosis and Ferroptosis in Diffuse Large B-Cell Lymphoma via NF-κB Inactivation.","authors":"Han-Shuo Zhang, Xiao-Dan Zhou, Jin Chen, Ling Wang","doi":"10.1002/kjm2.70110","DOIUrl":"https://doi.org/10.1002/kjm2.70110","url":null,"abstract":"<p><p>Diffuse large B-cell lymphoma (DLBCL) is the most common non-Hodgkin lymphoma and is an aggressive and highly heterogeneous tumor. Kaempferitrin (KPF) is a natural flavonoid glycoside that exerts a protective role in multiple human tumors. However, the impact of KPF on DLBCL remains unclear. In this study, we discovered that 240 μM KPF had a toxic effect on GM12878 cells. KPF inhibited DLBCL cell proliferation while promoting apoptosis in these cells. Additionally, KPF induced ferroptosis in DLBCL cells by elevating intracellular Fe²⁺ levels and reactive oxygen species (ROS) levels, alongside reducing the protein levels of GPX4 and SLC7A11. Moreover, KPF suppressed the activation of NF-κB in DLBCL cells. Building upon this finding, we further validated that KPF reduced DLBCL cell malignant growth through the inhibition of NF-κB activation. Meanwhile, animal studies further suggested that KPF inhibited DLBCL proliferation in vivo, mainly through reduced subcutaneous tumor volume, tumor weight, and increased apoptosis levels in mice. Furthermore, KPF suppressed the disorder of DLBCL cancer tissue arrangement and decreased p-NF-κB and p-IKB-α protein levels in DLBCL subcutaneous tumor tissues. In summary, our findings suggested that KPF enhanced apoptosis and ferroptosis in DLBCL cells via the deactivation of the NF-κB signaling pathway.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70110"},"PeriodicalIF":3.1,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145202664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loganin, an Iridoid Glycoside, Alleviates Paclitaxel-Induced Skeletal Muscle Toxicity by Enhancing Mitochondrial Function, Boosting Antioxidant Defenses, and Reducing Cellular Senescence.","authors":"Yu-Fan Chuang, Cai-Rong Wu, Wan-Hsuan Chang, Ying-Jung Su, Hung-Te Hsu, Fan-Li Lin, Yi-Ching Lo","doi":"10.1002/kjm2.70117","DOIUrl":"https://doi.org/10.1002/kjm2.70117","url":null,"abstract":"<p><p>Mitochondrial dysfunction and energy imbalance caused by chemotherapy are key contributors to skeletal muscle atrophy, which severely impacts the quality of life in cancer patients. Paclitaxel, a commonly used chemotherapeutic agent, is known to promote muscle wasting and cellular senescence, largely by impairing mitochondrial function. In this study, we investigated the protective role of loganin, a naturally occurring iridoid glycoside, in preventing paclitaxel-induced damage to skeletal muscle cells. Using C2C12 cells, we assessed whether loganin could counteract the harmful effects of paclitaxel. Our results demonstrated that loganin significantly improved cell viability and protected mitochondrial function, as reflected by better preservation of mitochondrial DNA content, membrane potential, and ATP production, while further enhancing mitochondrial biogenesis through upregulation of PGC-1α, TFAM, and NRF1. In parallel, loganin activated metabolic regulators SIRT1 and AMPK, while restoring PDK4 expression, suggesting improved energy regulation. Additionally, glycogen levels and myotube morphology were maintained, alongside sustained myosin heavy chain expression. Loganin effectively reduced both cellular and mitochondrial reactive oxygen species and increased antioxidant defenses, including superoxide dismutase activity and glutathione levels. Notably, it also suppressed paclitaxel-induced senescence and inflammation, as shown by decreased p21 expression, reduced NFκB phosphorylation, and lower levels of Cdkn1a and Il6 as well as reduced SA-β-gal staining. Overall, our findings demonstrate that loganin offers comprehensive protection against paclitaxel-induced skeletal muscle injury by preserving mitochondrial function, supporting metabolic homeostasis, reducing oxidative stress, and limiting senescence. These results highlight the potential of loganin as a preventive adjunctive agent to mitigate chemotherapy-related muscle toxicity.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70117"},"PeriodicalIF":3.1,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180807","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Time Since Diagnosis and Age on Fracture Risk in Young Adults With Type 1 and Type 2 Diabetes.","authors":"Tien-Ching Lee, Sung-Yen Lin, Chung-Hwan Chen, Pei-Shan Ho","doi":"10.1002/kjm2.70112","DOIUrl":"https://doi.org/10.1002/kjm2.70112","url":null,"abstract":"","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70112"},"PeriodicalIF":3.1,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Breast Milk-Derived Exosomal FP671120.4 Inhibits Macrophage M1 Polarization via Modulating the ELAVL1/Nrf2 Axis in Sepsis-Associated Liver Injury.","authors":"Zhao-Bin Yang, Yi-Bin Gao, Xiao-Mei Cheng, Lu-Zhen Qiu","doi":"10.1002/kjm2.70108","DOIUrl":"https://doi.org/10.1002/kjm2.70108","url":null,"abstract":"<p><p>Sepsis-associated liver injury (SALI) plays a major role in aggravating disease progression and worsening prognosis in patients with sepsis. Macrophage polarization is a key factor in the modulation of SALI progression. Recent studies have shown that human breast milk-derived exosomes (HBM-Exos) regulate processes involved in macrophage polarization. Here, we investigated the function and mechanism of action of HBM-Exos in a macrophage polarization model of SALI. The extracted HBM-Exos were identified by morphological analysis and detection of marker proteins using flow cytometry. Human Kupffer cells were treated with lipopolysaccharide (LPS) to simulate macrophage polarization in SALI. Cell viability was measured using a CCK-8 kit. Protein and gene expression levels were evaluated using western blotting and RT-qPCR, respectively. ELISA kits were used to assess the levels of inflammatory cytokines. The interactions between FP671120.4, ELAV Like RNA binding protein 1 (ELAVL1), and nuclear factor erythroid 2-related factor 2 (Nrf2) were verified by RIP analysis. HBM-Exos inhibited M1 macrophage polarization by promoting Nrf2 expression and phosphorylation via activation of the Nrf2/Heme oxygenase-1 (HO-1) signaling pathway in LPS-induced Kupffer cells. Furthermore, FP671120.4 reversed the HBM-Exos-mediated increase in Nrf2 mRNA stability. HBM-Exos-derived FP671120.4 enhanced the interaction between ELAVL1 and Nrf2. As a result, FP671120.4 inhibited M1 polarization by inducing Nrf2 expression via activation of the Nrf2/HO-1 pathway. These findings suggest that HBM-Exos-derived FP671120.4 may inhibit M1 macrophage polarization through the ELVAL1/Nrf2/HO-1 signaling pathway in LPS-induced Kupffer cells.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70108"},"PeriodicalIF":3.1,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Phase IIb Trial for the Palliative Treatment of Patients With Primary Hepatic Malignancy Unable to Receive Curative Treatment: Efficacy of Colchicine.","authors":"Zu-Yau Lin, Ming-Lun Yeh, Po-Cheng Liang, Shinn-Cherng Chen, Chung-Feng Huang, Jee-Fu Huang, Chia-Yen Dai, Ming-Lung Yu, Wan-Long Chuang","doi":"10.1002/kjm2.70121","DOIUrl":"https://doi.org/10.1002/kjm2.70121","url":null,"abstract":"<p><p>This trial was to evaluate the efficacy and the safety of colchicine for the palliative treatment of patients with primary hepatic malignancy unable to receive curative treatment. Forty hepatocellular carcinoma (HCC) patients and two intrahepatic cholangiocarcinoma (ICC) patients signed the informed consents. Most HCC participants (97%) had failed in tyrosine kinase inhibitor (TKI) and/or immunotherapy before entering the study. Colchicine was started from 1 mg twice per day and was adjusted ranging from 1.5 to 3 mg/day. One treatment cycle was defined as four continuous treatment days followed by 3 days off. The HCC control group was matched to the same condition (Child score, tumor staging, previous TKI, and/or immunotherapy) as the participants at a ratio of 3 to 1 (control to colchicine). The ICC control group was matched to the same tumor staging as the participants. The primary objective was to compare the survival between the two groups. The safety objective was to observe the adverse events of colchicine. The colchicine HCC group demonstrated longer median survival (283 days) than the control group (107 days) (p < 0.0001, 95% confidence interval 2.001-3.289, hazard ratio 0.3513, 95% confidence interval 0.2611-0.5523). Two ICC participants survived 491 and 461 days, respectively, compared to the control group with a median survival of 8.5 months and a 41.5% one-year survival rate. Diarrhea (5%) was the only directly colchicine-related grade 3-4 adverse event. In conclusion, this colchicine dosage schedule is clinically feasible as an effective palliative treatment for patients with primary hepatic malignancy unable to receive curative treatment. Trial Registration: ClinicalTrials.gov identifier: NCT04264260.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70121"},"PeriodicalIF":3.1,"publicationDate":"2025-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145180795","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In Vitro Evaluation of the Inhibitory Effects of Linarin on Histamine-Induced Expression of Proinflammatory Cytokines, Mucin 5AC, and Aquaporin 5 in Human Nasal and Bronchial Epithelial Cells.","authors":"Xin-Jing Mi, Jie Wang, Jian-Qiang Qi","doi":"10.1002/kjm2.70114","DOIUrl":"https://doi.org/10.1002/kjm2.70114","url":null,"abstract":"<p><p>Allergic rhinitis and asthma are two prevalent chronic allergic conditions in children. Linarin, a glycosylated flavonoid derived from various plants, exhibits a wide range of biological activities. This study aimed to investigate the therapeutic potential of linarin against allergic rhinitis and asthma. In vitro models of allergic rhinitis and asthma were established using human nasal epithelial cells (hNECs) and human bronchial epithelial cells (BEAS-2B), respectively. Linarin treatment inhibited histamine-induced increases in the expression levels of p-p65 and p-IκBα in whole-cell lysates, as well as p65 in nuclear lysates. The histamine-induced activation of MAPK pathways was suppressed by linarin, as evidenced by reduced phosphorylation ratios of ERK (pERK/ERK), JNK (pJNK/JNK), and p38 (pp38/p38). ELISA results further revealed that linarin attenuated histamine-induced secretion of proinflammatory cytokines, including IL-6, IL-8, and MCP-1. Western blot and RT-PCR analyses showed that linarin reversed histamine-induced MUC5AC upregulation and AQP5 downregulation. Notably, the inhibitory effects of linarin were potentiated in the presence of specific inhibitors targeting NF-κB (PDTC), ERK (U0126), p38 (SB203580), and JNK (SP600125). Collectively, these findings demonstrate that linarin suppresses histamine-induced proinflammatory cytokine secretion, MUC5AC upregulation, and AQP5 downregulation in human nasal and bronchial epithelial cells. These effects are mediated through the inhibition of the NF-κB and MAPK pathways. Thus, linarin may serve as a promising therapeutic agent for the treatment of allergic rhinitis and asthma.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70114"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Clinical Outcomes in Patients With T4b Esophageal Squamous Cell Carcinoma: A 10-Year Single Institution Experience.","authors":"Yi-Hsun Chen, Wen-Hung Hsu, I-Chen Wu, Pen-Tzu Fang, Song-Wei Wang, Chao-Chin Hsu, Yao-Kuang Wang","doi":"10.1002/kjm2.70116","DOIUrl":"https://doi.org/10.1002/kjm2.70116","url":null,"abstract":"<p><p>Esophageal squamous cell carcinoma (ESCC) with adjacent structure invasion (T4b), affecting areas such as the aorta, vertebral body, or trachea, is associated with a poor prognosis, and the optimal treatment strategy remains unclear. While chemotherapy is considered standard, radiation therapy is often avoided due to the risk of severe complications, including tracheoesophageal fistula. This 10-year cohort study investigated clinical outcomes and prognostic factors in patients with T4b ESCC. From October 2011 to May 2022, 471 ESCC patients were diagnosed at our institution, of whom 130 (27%) had T4b disease. First-line treatments included definitive chemoradiotherapy (n = 82), chemotherapy alone (n = 15), radiotherapy alone (n = 5), immunotherapy clinical trials (n = 7), palliative surgery (n = 2) and best supportive care (n = 19). Patients treated with definitive chemoradiotherapy demonstrated significantly longer overall survival compared with those receiving monotherapy. The mean survival was 24.2 months in the chemoradiotherapy group, versus 4.2 months with chemotherapy alone and 8.5 months with radiotherapy alone (p < 0.001). Esophageal fistula developed in 22 patients (16.9%), with 5 cases identified at diagnosis and 17 occurring during follow-up. Chemotherapy alone was associated with a significantly higher risk of fistula formation compared with chemoradiotherapy (adjusted hazard ratio = 11.22, p = 0.01). The presence of a fistula was correlated with worse survival outcomes (median survival of 8.9 months versus 12.2 months, p = 0.03). These findings suggest that definitive chemoradiotherapy may enhance survival in T4b ESCC patients.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70116"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152452","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Involvement of the miR-128-3p/KDM3A/NLRP3 Axis in High Glucose-Induced Inflammatory Injury in Retinal Endothelial Cells.","authors":"Wei-Ming Wen, Jian-Bo Feng, Yin-Sheng Cai, Nan Lin, Fei Lv, Zhu-Sheng Guo","doi":"10.1002/kjm2.70120","DOIUrl":"https://doi.org/10.1002/kjm2.70120","url":null,"abstract":"<p><p>This study explores the regulatory mechanism of the miR-128-3p in diabetic retinopathy (DR)-associated inflammatory injury. A cellular model of DR was established by inducing immortalized human retinal endothelial cells (IM-HRECs) with high-glucose (HG). Cell viability was evaluated by CCK-8 assay, and the levels of TNF-α, IL-1β, and IL-10 were measured by ELISA. RT-qPCR was performed to determine miR-128-3p expression, and miR-128-3p mimics were transfected into cells to verify its regulatory role in DR-associated inflammatory injury. miR-128-3p was predicted by Starbase to bind to the 3' UTR of KDM3A, which was verified by dual-luciferase assay. The expressions of KDM3A and NLRP3 in cells were examined by Western blotting, and the enrichment of KDM3A and H3K9me2 on the NLRP3 promoter was measured by Ch-IP assay. The results revealed that HG treatment significantly reduced both IM-HREC viability and IL-10 levels, increased the levels of TNF-α and IL-1β, and downregulated the expression of miR-128-3p. Overexpression of miR-128-3p reduced inflammation in IM-HRECs induced by HG. The proposed mechanism involves targeting of the KDM3A 3' UTR by miR-128-3p, leading to reduced KDM3A expression, while KDM3A increased NLRP3 expression by reducing H3K9me2. In conclusion, upregulation of miR-128-3p increases the histone H3K9me2 level by inhibiting KDM3A expression, thereby reducing NLRP3 expression and suppressing DR inflammatory injury.</p>","PeriodicalId":94244,"journal":{"name":"The Kaohsiung journal of medical sciences","volume":" ","pages":"e70120"},"PeriodicalIF":3.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145152583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}