MedScience最新文献_第6页

Exposure to high altitude: a potential driver of accelerated biological aging. 暴露于高海拔：加速生物老化的潜在驱动因素。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-02-14 DOI: 10.1007/s11684-025-1195-6

Xingkai Zhang, Qinghai Shi

引用次数: 0

Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer. RNA修饰阅读器YTHDF2在造血、免疫和癌症中的新作用。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-04-01 DOI: 10.1007/s11684-026-1203-5

Xin Liu, Sai Xiao, Songqi Duan, Jianjun Chen, Shoubao Ma

{"title":"Emerging role of RNA modification reader YTHDF2 in hematopoiesis, immunity, and cancer.","authors":"Xin Liu, Sai Xiao, Songqi Duan, Jianjun Chen, Shoubao Ma","doi":"10.1007/s11684-026-1203-5","DOIUrl":"10.1007/s11684-026-1203-5","url":null,"abstract":"N6-methyladenosine (m6A) RNA modification has emerged as a pivotal epitranscriptomic mark shaping RNA metabolism and cellular programs. Among the diverse m6A reader proteins, YTHDF2 has garnered significant attention as a key regulator of RNA stability. Recent studies highlight the multifaceted roles of YTHDF2 in orchestrating hematopoietic stem cell self-renewal and differentiation, fine-tuning immune cell development and function, and modulating tumor-immune interactions within the tumor microenvironment. YTHDF2 has also been shown to function as a reader for RNA 5-methylcytosine (m5C) modification. By linking m6A- and/or m5C-dependent RNA dynamics to hemato-immune homeostasis, YTHDF2 functions as a central epitranscriptomic integrator linking intrinsic genetic programs to developmental and environmental cues. Here, we summarize current advances in understanding YTHDF2-mediated RNA regulation across physiological and pathological contexts, discuss its potential as a therapeutic target in immune-related diseases and cancers, and highlight future directions in the field.","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"59-77"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13060541/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597816","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

Electroacupuncture at ST36 protects against dextran sulfate sodium-induced ulcerative colitis in mice by enhancing sympathetic nerve innervation in colonic tissue. 电针ST36部位通过增强结肠组织交感神经支配，对小鼠葡聚糖硫酸钠诱导的溃疡性结肠炎有保护作用。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-03-31 DOI: 10.1007/s11684-025-1198-3

Dongfeng Zhao, Yuquan Yang, Junhao Liang, Chuanglong Xu, Chunlan Tang, Mingming Zhang, Chenguang Li, Yongjian Zhao, Bing Shu, Wei Gou, Yongjun Wang

{"title":"Electroacupuncture at ST36 protects against dextran sulfate sodium-induced ulcerative colitis in mice by enhancing sympathetic nerve innervation in colonic tissue.","authors":"Dongfeng Zhao, Yuquan Yang, Junhao Liang, Chuanglong Xu, Chunlan Tang, Mingming Zhang, Chenguang Li, Yongjian Zhao, Bing Shu, Wei Gou, Yongjun Wang","doi":"10.1007/s11684-025-1198-3","DOIUrl":"10.1007/s11684-025-1198-3","url":null,"abstract":"Ulcerative colitis (UC), characterized by diffuse colonic inflammation and enteric nervous system (ENS) alterations, remains a therapeutic challenge. While the role of the parasympathetic nervous system in intestinal inflammation has been extensively documented, understanding of sympathetic nervous system (SNS) function in UC pathogenesis remains limited. Electroacupuncture (EA) at ST36 (Zusanli) is a widely used alternative therapy for UC, yet its regulatory effects on the ENS-particularly the SNS-and the underlying mechanisms remain unclear. Here, we established a 2.5% dextran sulfate sodium (DSS)-induced murine UC model and validated disease phenotypes via histological assessment. Using a non-anesthetic EA intervention protocol mimicking the clinical conditions, we found that EA at ST36 attenuated local inflammatory progression in DSS-induced UC mice and mitigated ENS degeneration. Critically, our results demonstrated that EA at ST36 specifically reversed SNS reduction (tyrosine hydroxylase-positive, TH+ neurons) in colonic tissue caused by intestinal inflammation. In conclusion, this study reveals that EA at ST36 restores colonic homeostasis through a sympathetic-dependent mechanism, providing novel insights and therapeutic strategies for the clinical management of UC.","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"164-172"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147597802","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}

引用次数: 0

Targeting Nrf3-Pitx2-ROS axis represents a promising therapeutic strategy for myocardial infarction. 靶向Nrf3-Pitx2-ROS轴是一种很有前景的心肌梗死治疗策略。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-02-14 DOI: 10.1007/s11684-025-1194-7

Min Zhang, Hui He, Zhen He, Jin Zou, Xiaobo Hu

引用次数: 0

High-altitude exposure remodels the gut microbiota: health and disease. 高海拔暴露重塑了肠道菌群：健康和疾病。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-03-27 DOI: 10.1007/s11684-026-1206-2

Yan Li, Mingshan Jiang, Jiangmei Pang, Chunxiang Ma, Hong Zhang, Fang Yin, Yongbin Jia, Xiang Zou, Tao Zuo, Hu Zhang

{"title":"High-altitude exposure remodels the gut microbiota: health and disease.","authors":"Yan Li, Mingshan Jiang, Jiangmei Pang, Chunxiang Ma, Hong Zhang, Fang Yin, Yongbin Jia, Xiang Zou, Tao Zuo, Hu Zhang","doi":"10.1007/s11684-026-1206-2","DOIUrl":"10.1007/s11684-026-1206-2","url":null,"abstract":"With the increasing number of individuals travelling to or residing in high-altitude regions, understanding the physiological and pathological consequences of such environments has become increasingly important. High-altitude exposure poses significant challenges to human health, primarily due to hypobaric hypoxia, which triggers a cascade of responses, including energy deficiency, oxidative stress, and inflammation. One of the critical consequences is the disruption of the gut barrier, which facilitates the translocation of the gut microbiota and further exacerbates local and systemic inflammation. Notably, the gut microbiota, a dynamic environmental sensor, undergoes significant remodelling in high-altitude environments. The modified production of microbial metabolites such as bile acids influences gut homeostasis as well as glucose and lipid metabolism, and ultimately contributes to individual variability in high-altitude acclimatization. These changes have been implicated in the pathogenesis of altitude-related illnesses such as acute and chronic mountain sickness, as well as in metabolic and gastrointestinal disorders such as diabetes, obesity, irritable bowel syndrome, colorectal cancer, cholelithiasis, and osteoporosis. Preliminary explorations have demonstrated the therapeutic potential of microbiome-based interventions such as faecal microbiota transplantation in acute and chronic mountain sickness. Further research into gut microbiota modulation may provide applicable options for promoting high-altitude acclimatization and preventing high-altitude illness.","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"120-146"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147535668","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}

引用次数: 0

Qizaobaoxin Decoction ameliorates doxorubicin/trastuzumab-induced cardiotoxicity by modulating gut microbiota and associated metabolites. 七杂保心汤通过调节肠道菌群和相关代谢物改善阿霉素/曲妥珠单抗诱导的心脏毒性。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-02-16 DOI: 10.1007/s11684-025-1196-5

Mengmeng Lin, Shizhang Wei, Bo Cao, Zhihong Wang, Peizhi Ye, Chunyu Li, Guohui Li

{"title":"Qizaobaoxin Decoction ameliorates doxorubicin/trastuzumab-induced cardiotoxicity by modulating gut microbiota and associated metabolites.","authors":"Mengmeng Lin, Shizhang Wei, Bo Cao, Zhihong Wang, Peizhi Ye, Chunyu Li, Guohui Li","doi":"10.1007/s11684-025-1196-5","DOIUrl":"10.1007/s11684-025-1196-5","url":null,"abstract":"Sequential treatment with anthracyclines and trastuzumab is highly effective for HER-2 positive breast cancer but poses a significant risk of cardiotoxicity. Qizaobaoxin Decoction (QZBXD), a modified Chinese herbal formula, has shown promise in protecting against antineoplastic drug-induced cardiotoxicity. This study aimed to investigate the chemical composition, efficacy, and mechanisms of QZBXD in mitigating doxorubicin/trastuzumab (DOX/TRZ)-induced cardiotoxicity. Using UPLC-Q-TOF-MS/MS, 83 compounds in QZBXD were identified, including flavonoids, organic acids, and phthalides. In DOX/TRZ-induced cardiotoxicity model, QZBXD treatment improved cardiac function (increased left ventricular ejection fraction and left ventricular fractional shortening), reduced biomarkers of myocardial injury (cTnI, BNP, LDH, CK-MB, α-HBDH), and alleviated histopathological damage. Mechanistically, 16S rDNA sequencing revealed that QZBXD restored gut microbiota diversity, reducing harmful bacteria (Ruminococcus, Oscillibacter) and increasing beneficial bacteria (Bacteroides). Untargeted metabolomics showed that QZBXD modulated tryptophan and arachidonic acid metabolism, affecting key metabolites (e.g., decreasing tryptamine and 8,9-epoxyeicosatrienoic acid, and increasing 4-hydroxy-L-tryptophan and L-formylkynurenine). Integrated analysis revealed that QZBXD confers cardioprotective effects against DOX/TRZ-induced cardiotoxicity by modulating gut microbiota composition, which subsequently influences tryptophan and arachidonic acid metabolism. This study provides a pharmacological basis for the clinical application of QZBXD in mitigating DOX/TRZ-induced cardiotoxicity.","PeriodicalId":521275,"journal":{"name":"MedScience","volume":" ","pages":"147-163"},"PeriodicalIF":0.0,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147287006","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}

引用次数: 0

Advances in multi-omics and aging clock research for female reproductive health and aging. 女性生殖健康与衰老的多组学与衰老时钟研究进展。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-03-27 DOI: 10.1007/s11684-026-1207-1

Rui Wang, Yaqian Li, Lan Zhu

引用次数: 0

Profound changes in frontiers of medicine and promotion of MedScience. 医学前沿的深刻变化和医学科学的促进。

MedScience Pub Date : 2026-02-01 Epub Date: 2026-04-20 DOI: 10.1007/s11684-026-1252-9

Sai-Juan Chen, Boli Zhang, Xiao-Fan Wang

引用次数: 0