Clinical and Experimental Medicine最新文献

{"title":"Elevated expression of transferrin receptor-1 in pancreatic cancer: clinical implications and prognostic significance.","authors":"Li Zhongqing, Shahab Uddin, Zhou Wence","doi":"10.1007/s10238-025-01847-0","DOIUrl":"https://doi.org/10.1007/s10238-025-01847-0","url":null,"abstract":"<p><strong>Purpose: </strong>Many advanced-stage pancreatic cancers are fatal, highlighting the need for solid prognostic indicators. This study evaluates transferrin receptor-1 (TfR1) expression in pancreatic cancer tissues and cell lines for clinical and therapeutic potential.</p><p><strong>Method: </strong>The GuangRe database, which integrates mRNA data from The Cancer Genome Atlas (TCGA) and the Genotype-Tissue Expression (GTEx) project, was used to assess TFRC gene expression in pancreatic cancer and normal tissues. ROC curves and Kaplan-Meier and Log-rank tests were used to evaluate TFRC gene expression's diagnostic and survival efficacy. In vitro Western blotting and immunofluorescence experiments on pancreatic cancer cell lines assessed TfR1 expression. IHC staining was done on tissue samples from 90 patients to determine TfR1's clinical importance.</p><p><strong>Results: </strong>The study found that TFRC mRNA levels were significantly higher in pancreatic cancer tissues compared to nearby normal tissues (P < 0.05), with an AUC of 0.936. We found higher TfR1 protein levels in pancreatic cancer cell lines (P < 0.01) using western blot and immunofluorescence studies. Immunohistochemistry showed that pancreatic cancer tissues expressed 30.1% TfR1 compared to paracancer (11.1%) (P = 0.003). In COX regression analysis, increased TfR1 expression was related with lower overall survival (OS) and progression-free survival (PFS), making it an independent prognostic factor.</p><p><strong>Conclusion: </strong>Higher TfR1 expression is associated with poor pancreatic cancer outcomes, suggesting its potential as a prognostic biomarker and therapeutic target.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"307"},"PeriodicalIF":3.5,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12394385/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of exercise on immune cell infiltration in muscle tissue: implications for muscle repair and chronic disease.","authors":"Yiping Su, Zhanguo Su","doi":"10.1007/s10238-025-01852-3","DOIUrl":"https://doi.org/10.1007/s10238-025-01852-3","url":null,"abstract":"<p><p>Exercise has long been recognized for its systemic health benefits, including modulation of the immune system. Contemporary scientific inquiry has increasingly turned toward understanding the regulatory effects of exercise on immune cell dynamics within muscle tissue, highlighting their potential role in facilitating tissue repair and modulating chronic disease pathways. Following acute bouts of exercise, especially those involving eccentric or high-intensity contractions, muscle fibers experience micro-damage that triggers a well-orchestrated immune response. This phenomenon entails a coordinated, time-sensitive accumulation of immune effector cells-namely neutrophils, macrophages, and T lymphocytes-within compromised muscle tissue. Through the release of immunoregulatory and regenerative mediators like cytokines and growth factors, these cells actively participate in coordinating tissue repair by eliminating cellular debris and resolving inflammation.Macrophage polarization from a pro-inflammatory (M1) to an anti-inflammatory (M2) phenotype is particularly crucial in coordinating effective muscle repair and preventing fibrosis. However, dysregulation of this immune response, such as persistent inflammation or impaired immune cell transition, can hinder regeneration and contribute to the pathogenesis of chronic conditions like sarcopenia, insulin resistance, and muscular dystrophies. Moreover, in chronic disease states, immune cell infiltration into muscle may become maladaptive, exacerbating tissue damage and metabolic dysfunction.Regular moderate-intensity exercise appears to modulate this immune infiltration in a way that enhances repair mechanisms while reducing chronic inflammation, highlighting a potential therapeutic avenue for managing muscle-related pathologies. In-depth insight into the molecular and cellular crosstalk between physical activity and immune cell regulation in muscle tissue forms the basis for crafting specialized therapeutic strategies aimed at facilitating muscle regeneration and limiting the development of chronic pathological conditions. Through a detailed evaluation of exercise-elicited immune dynamics, this review underscores the dichotomous functions of immune cell infiltration in supporting muscle regeneration and in contributing to strategies for chronic disease prevention and management.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"306"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12391213/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The shared genetic etiology of autoimmune disorders and interstitial lung disease: insights from large-scale genome-wide cross-trait analysis.","authors":"Fang Zhou, Ting Li, Hongyan Hui, Jianlian Gao, Zhichao Xu, Zhijian Deng","doi":"10.1007/s10238-025-01836-3","DOIUrl":"https://doi.org/10.1007/s10238-025-01836-3","url":null,"abstract":"<p><p>Autoimmune diseases often co-occur with interstitial lung disease (ILD), and ILD is associated with patient prognosis. Research has demonstrated a relationship between autoimmune diseases and ILD; however, the genetic basis underlying this connection is frequently overlooked. Linkage disequilibrium score regression and high-definition likelihood methods were applied to large-scale genome-wide association studies summary-level data sets to assess genetic correlations between 17 autoimmune disorders and ILD. Several functional annotations and tissue-specific analyses were performed to determine the influence of pleiotropic genes based on the pleiotropy analysis method under the compound null hypothesis method. Eight autoimmune disorders were revealed sharing genetic mechanisms with ILD. A total of 107 pleiotropic loci were identified at the genome-wide significance level (P < 5 × 10^-8), 18 of which had strong evidence of colocalization. Multiple potential pleiotropic genetic loci were identified, particularly the SMO gene located 7q32.1 locus. Pathway analysis determined in bound by FOXP3, T cell selection, and regulation of immune response. SNP- and gene-level tissue enrichment revealed that pleiotropic mechanisms play a critical role in spleen, whole blood, lung, and EBV-transformed lymphocytes. There are significant genetic correlations and potential causal mechanisms between autoimmune diseases and ILD. The findings of this study provide a deeper understanding of the genetic architecture of autoimmune diseases and ILD.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"305"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12391177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945236","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SLFN11, far from being limited to responding to cancer DNA damage.","authors":"Hao Xiao, Zeping Han, Yingkai Tang, Xukang Gao, Min Xu, Shuangjian Qiu, Ning Ren, Yong Yi, Chenhao Zhou","doi":"10.1007/s10238-025-01776-y","DOIUrl":"https://doi.org/10.1007/s10238-025-01776-y","url":null,"abstract":"<p><p>SLFN11, a member of the evolutionarily conserved SLFN gene family, is an interferon-stimulated early response gene. This review comprehensively explores its multifaceted roles. Structurally, its three distinct domains endow it with diverse functions. Epigenetic modifications, post-translational alterations, and multiple signaling pathways intricately regulate SLFN11 expression and activity. In terms of functions, it plays crucial roles in the DNA damage response during replication stress, distinct from traditional pathways. It also serves as a protector in the antiviral response and a valuable biomarker for predicting the efficacy of DNA-damaging agents and patient prognosis in various cancers. Beyond these, SLFN11 has non-canonical functions, including immune regulation, modulation of oncological behaviors, involvement in apoptosis, protection against proteotoxic stress, and association with Fanconi anemia. Looking ahead, SLFN11 holds great promise as a biomarker for personalized medicine, but challenges like developing accurate detection methods remain. In immunotherapy, understanding its dynamic changes is essential for optimizing treatment. Strategies to overcome SLFN11-low expression, such as epigenetic modulation, also need further investigation, which may open new avenues for disease treatment.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"304"},"PeriodicalIF":3.5,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12380651/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel prognostic signature integrating disulfidptosis- and ferroptosis-related genes in acute myeloid leukemia.","authors":"Huihui Jiang, Li Liang, Tingting Liu, Zhe Zhao, Nana Wang, Jingtao Wang, Yuanyuan Hu, Dongmei Wang, Jingjing Ye, Fei Lu, Chunyan Ji","doi":"10.1007/s10238-025-01670-7","DOIUrl":"https://doi.org/10.1007/s10238-025-01670-7","url":null,"abstract":"<p><p>Acute myeloid leukemia is a highly heterogeneous hematopoietic malignancy, and we constructed a prognostic signature combining disulfidptosis-related genes and ferroptosis-related genes to predict the prognosis, immunotherapy response, and drug sensitivity of acute myeloid leukemia (AML) patients. The TCGA-LAML datasets underwent random partitioning into training and validation sets. Subsequently, a prognostic risk signature was formulated using the least absolute shrinkage and selection operator algorithm. Kaplan-Meier survival analysis and receiver operating characteristic curve analysis were employed to assess the clinical significance of the signature. The results of the immune infiltration difference analyses are displayed, and the drug sensitivity analyses were used to identify potentially effective drugs for AML patients. qPCR was employed to validate the expression levels of the signature genes and compared the signature with existing signatures and mutated genes. Univariate and multivariate Cox regression analyses have underscored the signature as an autonomous prognostic risk determinant. Scrutiny into immune infiltration has unveiled significant associations: the risk score exhibits a favorable correlation with monocyte and M2 macrophage counts but an adverse correlation with resting mast cell counts. The expression patterns of immune checkpoint genes diverge between the distinct risk cohorts. Patients categorized as high-risk demonstrate enhanced benefits from cyclopamine, 443654, and 770041, whereas those classified as low-risk exhibit more pronounced advantages from cytarabine and AZD6244. The risk signature demonstrates superior prognostic accuracy compared to established signatures and mutated genes. In summary, our study may provide potential prognostic biomarkers and individualized precision therapy for AML patients.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"303"},"PeriodicalIF":3.5,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12378281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945168","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diagnostic utility and clinical relevance of anti-MCV and anti-CCP antibodies in rheumatoid arthritis.","authors":"Feng Dong, Limin Wang","doi":"10.1007/s10238-025-01850-5","DOIUrl":"https://doi.org/10.1007/s10238-025-01850-5","url":null,"abstract":"<p><p>Rheumatoid arthritis (RA) is a persistent autoimmune disorder where serological biomarkers play a crucial role in diagnosis and monitoring disease activity. Antibodies targeting cyclic citrullinated peptides (anti-CCP), mutated citrullinated vimentin (anti-MCV), and rheumatoid factor are commonly used serological markers for RA. However, their respective diagnostic efficacies and potential for mutual complementation remain incompletely understood. This study investigates the diagnostic performance of these three antibodies and their association with disease progression in RA. A total of 257 RA patients who visited Jinhua Hospital Affiliated with Zhejiang University between March and December 2019 were enrolled. Serum specimens were analyzed for anti-CCP, anti-MCV antibodies, and RF levels using chemiluminescence immunoassay (CLIA) and rate nephelometry. The results indicated that the specificity of anti-CCP (94.2%) was higher than that of anti-MCV (84.4%) and RF (84.8%). Furthermore, anti-MCV antibody levels were significantly link to disease duration and morning stiffness. Additionally, anti-MCV and anti-CCP demonstrated differing associations with extra-articular manifestations of RA. The study suggests that anti-MCV antibodies hold significant potential as adjunctive biomarkers in RA, complementing anti-CCP antibodies to improve diagnostic accuracy and provide new insights for early diagnosis and disease monitoring in RA.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"302"},"PeriodicalIF":3.5,"publicationDate":"2025-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12375518/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic options for extramedullary involvement in multiple myeloma.","authors":"Junmei Zhao, Yushan Cui, Baijun Fang","doi":"10.1007/s10238-025-01821-w","DOIUrl":"https://doi.org/10.1007/s10238-025-01821-w","url":null,"abstract":"<p><p>Extramedullary involvement (extramedullary disease, EMD) is an aggressive subtype of multiple myeloma (MM) characterized by myeloma subclones proliferating independently of the bone marrow microenvironment, often associated with high-risk cytogenetic abnormalities, immune evasion, and treatment resistance. While significant breakthroughs have been achieved in MM treatment with the sequential approval of proteasome inhibitors, immunomodulatory drugs, and anti-CD38 monoclonal antibodies, prognosis remains poor once EMD develops. Even in the era of immunotherapy, the survival benefit for EMD patients has not shown significant improvement. This review systematically summarizes therapeutic options for MM patients with EMD, aiming to provide evidence-based guidance for EMD treatment.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"301"},"PeriodicalIF":3.5,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12374916/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevalence and outcome of VEXAS syndrome in unrelated hematopoietic cell transplantation for bone marrow failure.","authors":"Yoshitaka Zaimoku, Tatsuya Imi, Tatsuya Hatada, Hiroki Mizumaki, Hiroki Mura, Hiroki Yoshino, Yui Kano, Miku Kobayashi, Eriko Morishita, Natsumi Fushida, Takashi Matsushita, Keishi Mizuguchi, Hiroko Ikeda, Yasuhito Nannya, Seishi Ogawa, Kazuyoshi Hosomichi, Noriko Doki, Yuta Katayama, Takashi Koike, Ken-Ichi Matsuoka, Tetsuya Nishida, Yoshiyuki Takahashi, Keisuke Kataoka, Hideyuki Nakazawa, Yasunori Ueda, Takahiro Fukuda, Tatsuo Ichinohe, Fumihiko Ishimaru, Makoto Onizuka, Yoshiko Atsuta, Toshihiro Miyamoto","doi":"10.1007/s10238-025-01832-7","DOIUrl":"https://doi.org/10.1007/s10238-025-01832-7","url":null,"abstract":"<p><p>VEXAS syndrome (vacuoles, E1 enzyme, X-linked, autoinflammatory, and somatic) is a recently identified clonal disorder caused by somatic UBA1 mutations in hematopoietic stem cells, leading to bone marrow failure (BMF) and systemic inflammation. We screened 1771 patients with BMF who underwent unrelated hematopoietic cell transplantation in Japan between 1995 and 2020 using multitarget real-time PCR. The diagnoses included myelodysplastic syndrome (MDS, n = 1139), myeloproliferative neoplasms (n = 125), plasma cell neoplasms (n = 23), acquired BMF (n = 395), and congenital BMF (n = 89). Pathogenic UBA1 mutations were detected in two male patients with MDS (aged 48 and 63 years), corresponding to a prevalence of 0.11% in the overall cohort and 0.18% in MDS cases; an additional 70-year-old male was diagnosed outside of the cohort. All three underwent unrelated bone marrow transplantation following fludarabine and busulfan-based conditioning. The first and third patients died of idiopathic pneumonia syndrome 5 and 28 months after transplantation. In the third patient, UBA1-mutant cells persisted at low frequency in skin graft-versus-host disease tissue despite clearance from his blood. The second patient survived without relapse or graft-versus-host disease at 28 months. Although VEXAS syndrome is rare among unrelated HCT recipients with malignant and non-malignant BMF in the historical cohort, HCT is positioned as a potentially curative, yet high-risk strategy. Additional studies are essential to refine patient selection, optimize transplant timing, and improve management strategies to mitigate risk and enhance survival. Therefore, the role of tissue-residual UBA1-mutant clones in post-transplant complications warrants further investigation.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"300"},"PeriodicalIF":3.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373688/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Efficacy of combination chelation with deferasirox and deferiprone in children with beta-thalassemia major: an audit from a unit in the developing world.","authors":"Vinson James, Anand Prakash","doi":"10.1007/s10238-025-01687-y","DOIUrl":"https://doi.org/10.1007/s10238-025-01687-y","url":null,"abstract":"<p><p>Effective iron chelation is crucial for preventing morbidity and mortality in transfusion-dependent beta-thalassemia major. While oral chelation is the preferred mode of administration, heavily iron-overloaded patients often require combination therapy. Although desferoxamine and deferiprone are commonly recommended, a combination of two oral chelators-deferasirox and deferiprone, offers a more convenient alternative. This study evaluates the efficacy and safety of combination oral chelation in pediatric patients with severe iron overload. Children with transfusion-dependent beta-thalassemia major and persistently high serum ferritin levels (> 2500 µg/dL) for more than six months despite maximum-dose deferasirox (40 mg/kg/day) were initiated on combination chelation with deferiprone. Serum ferritin levels were monitored at six-month intervals to assess treatment efficacy. Among 130 regularly followed patients, 27 met the criteria for combination chelation. A significant reduction in serum ferritin levels was observed, decreasing from 4277 ± 1885 µg/dL at baseline to 3242 ± 1110 µg/dL at six months (p = 0.003) and further to 2985 ± 1116 µg/dL at twelve months (p = 0.018). No significant adverse effects were noted during the study period. Combination chelation with deferasirox and deferiprone is an effective and well-tolerated strategy for managing severe iron overload in children with beta-thalassemia major. This approach provides a practical alternative to injectable therapies and may improve adherence and treatment outcomes.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"299"},"PeriodicalIF":3.5,"publicationDate":"2025-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373522/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The association between 4-HPR-mediated LCN2 suppression and reduced intestinal cell senescence in ulcerative colitis.","authors":"Xiaoxue Pan, Jianghao Wang, Jing Zhu, Xin Wang, Yucun Liu, Shanwen Chen, Pengyuan Wang","doi":"10.1007/s10238-025-01843-4","DOIUrl":"https://doi.org/10.1007/s10238-025-01843-4","url":null,"abstract":"<p><p>Ulcerative colitis is a type of inflammatory bowel disease that can significantly impact patients' life, leading to long-term complications. Cellular senescence plays a significant role in the occurrence and development of enteritis. The purpose of this study is to identify a specific drug and potential target that can inhibit intestinal cell senescence, thereby improving the clinical outcomes of enteritis. Bioinformatics analysis was used to identify the drug and target that associated with cellular senescence and ulcerative colitis. LPS-induced in vitro models and DSS-induced in vivo colitis models were used to confirm the association between colitis and aging, as well as the ability of the drug to alleviate colitis symptoms. Bioinformatics analysis suggested that Fenretinide (4-HPR) may influence the progression of ulcerative colitis by targeting LCN2 to modulate cellular senescence. Western blot analysis revealed high expression of LCN2 in patients with ulcerative colitis (p- value < 0.05). In the in vivo experiments utilizing a DSS-induced colitis model, 4-HPR was shown to be both safe and effective in inhibiting colitis progression. Western blot analysis indicated the downregulation of the senescence markers P16 and P21 following 4-HPR treatment (adjusted p-value < 0.0001). Moreover, β-galactosidase staining of intestinal tissues revealed a reduction in the accumulation of senescent cells in the 4-HPR-treated group compared to the DSS group (adjusted p-value < 0.0001). The potential mechanism might be related to the regulation of the Treg/Th17 balance. 4-HPR reduced the intestinal cell senescence by inhibiting the expression of LCN2 that alleviated the symptoms of ulcerative colitis.</p>","PeriodicalId":10337,"journal":{"name":"Clinical and Experimental Medicine","volume":"25 1","pages":"297"},"PeriodicalIF":3.5,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12370867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}