Journal of Biomedical Research最新文献

Upregulated inwardly rectifying K ⁺ current-mediated hypoactivity of parvalbumin interneuron underlies autism-like deficits in Bod1-deficient mice. 内向整流 K + 电流介导的副发光体中间神经元低活性上调是 Bod1 缺陷小鼠自闭症样缺陷的基础。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-03-25 DOI: 10.7555/JBR.38.20240394

Chen Li, Kerui Wang, Xingfeng Mao, Xiuxiu Liu, Yingmei Lu

{"title":"Upregulated inwardly rectifying K + current-mediated hypoactivity of parvalbumin interneuron underlies autism-like deficits in Bod1-deficient mice.","authors":"Chen Li, Kerui Wang, Xingfeng Mao, Xiuxiu Liu, Yingmei Lu","doi":"10.7555/JBR.38.20240394","DOIUrl":"https://doi.org/10.7555/JBR.38.20240394","url":null,"abstract":"Parvalbumin-positive (PV +) interneuron dysfunction is believed to be linked to autism spectrum disorder (ASD), a neurodevelopmental disorder, characterized by social deficits and stereotypical behaviors. However, the underlying mechanisms of PV + interneuron dysfunction remain largely unclear. Here, we found that a deficiency of biorientation defective 1 ( Bod1) in PV + interneuron led to an ASD-like phenotype in Pvalb-Cre; Bod1 f/f mice. Mechanistically, we identified that Bod1 deficiency induced hypoactivity of PV + interneuron and hyperactivity of calcium/calmodulin-dependent protein kinase Ⅱ alpha (CaMKⅡα) neurons in the medial prefrontal cortex (mPFC), as determined by whole-cell patch-clamp recording. Additionally, it concurrently decreased the power of high gamma oscillation, as assessed by in vivo multi-channel electrophysiological recording. Furthermore, we found that Bod1 deficiency enhanced inwardly rectifying K + current, leading to an increase in the resting membrane potential of PV + interneurons. Importantly, the gain-of-function of Bod1 improved social deficits and stereotypical behaviors in Pvalb-Cre; Bod1 f/f mice. These findings provide mechanistic insights into the PV + interneuron dysfunction and suggest new strategies for developing PV + interneuron therapies for ASD.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-13"},"PeriodicalIF":2.2,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752769","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets. 缺氧条件下心血管疾病的分子通路：机制、生物标志物和治疗靶点。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-03-20 DOI: 10.7555/JBR.38.20240387

Izzatullo Ziyoyiddin O G Li Abdullaev, Ulugbek Gapparjanovich Gayibov, Sirojiddin Zoirovich Omonturdiev, Sobirova Fotima Azamjonovna, Sabina Narimanovna Gayibova, Takhir Fatikhovich Aripov

{"title":"Molecular pathways in cardiovascular disease under hypoxia: Mechanisms, biomarkers, and therapeutic targets.","authors":"Izzatullo Ziyoyiddin O G Li Abdullaev, Ulugbek Gapparjanovich Gayibov, Sirojiddin Zoirovich Omonturdiev, Sobirova Fotima Azamjonovna, Sabina Narimanovna Gayibova, Takhir Fatikhovich Aripov","doi":"10.7555/JBR.38.20240387","DOIUrl":"https://doi.org/10.7555/JBR.38.20240387","url":null,"abstract":"Chronic hypoxia is a key factor in the pathogenesis of cardiovascular diseases, including ischemia, heart failure, and hypertension. Under hypoxic conditions, oxygen deficiency disrupts oxidative phosphorylation in mitochondria, impairing ATP production and generating reactive oxygen species (ROS). These reactive species induce mitochondrial dysfunction, leading to oxidative stress, calcium imbalance, and activation of apoptosis pathways. Mitochondrial K-ATP (mitoK-ATP) and mitochondrial permeability transition pore (mPTP) channels are particularly affected, contributing to membrane potential loss, cytochrome C release, and cell death. This review explores the molecular mechanisms underlying hypoxia-induced cardiovascular diseases, with a focus on mitochondrial impairment, ion channel dysfunction, and ROS overproduction. Additionally, we examine hypoxia-inducible factor 1-alpha (HIF-1α) as a biomarker of cellular adaptation and discuss therapeutic strategies targeting mitochondrial function and oxidative stress. Antioxidants and compounds modulating key ion channels, such as K-ATP and mPTP, are highlighted as promising interventions for mitigating hypoxia-induced damage. Furthermore, we emphasize the potential of integrating in vitro, in vivo, and in silico studies to develop novel therapies aimed at preserving mitochondrial integrity and preventing cardiovascular diseases.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-16"},"PeriodicalIF":2.2,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143692233","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Bidirectional Mendelian randomization and mediation analysis of million-scale data reveal causal relationships between thyroid-related phenotypes, smoking, and lung cancer. 双向孟德尔随机化和百万级数据的中介分析揭示了甲状腺相关表型、吸烟和肺癌之间的因果关系。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-02-25 DOI: 10.7555/JBR.38.20240421

Xiang Wang, Xuan Wang, Mengsheng Zhao, Lijuan Lin, Yi Li, Ning Xie, Yanru Wang, Aoxuan Wang, Xiaowen Xu, Can Ju, Qiuyuan Chen, Jiajin Chen, Ruili Hou, Zhongwen Zhang, David C Christiani, Feng Chen, Yongyue Wei, Ruyang Zhang

{"title":"Bidirectional Mendelian randomization and mediation analysis of million-scale data reveal causal relationships between thyroid-related phenotypes, smoking, and lung cancer.","authors":"Xiang Wang, Xuan Wang, Mengsheng Zhao, Lijuan Lin, Yi Li, Ning Xie, Yanru Wang, Aoxuan Wang, Xiaowen Xu, Can Ju, Qiuyuan Chen, Jiajin Chen, Ruili Hou, Zhongwen Zhang, David C Christiani, Feng Chen, Yongyue Wei, Ruyang Zhang","doi":"10.7555/JBR.38.20240421","DOIUrl":"https://doi.org/10.7555/JBR.38.20240421","url":null,"abstract":"Emerging evidence highlights the role of thyroid hormones in cancer, though findings are controversial. Research on thyroid-related traits in lung carcinogenesis is limited. Using UK Biobank data, we conducted bidirectional Mendelian randomization (MR) to assess causal links between lung cancer risk and thyroid dysfunction (hypothyroidism/hyperthyroidism) or function traits (free thyroxine [FT4], normal-range TSH). Furthermore, in the smoking-behavior stratified MR analysis, we evaluated the mediating effect of thyroid-related phenotypes on the association between smoking phenotype and lung cancer. We confirmed significant associations between lung cancer risk and hypothyroidism (hazards ratio [HR] = 1.14, 95% confidence interval [CI] = 1.03-1.26, P = 0.009) as well as hyperthyroidism (HR = 1.55, 95% CI = 1.29-1.87, P = 1.90×10 -6) in the UKB. Moreover, the MR analysis indicated a causal effect of thyroid dysfunction on lung cancer risk (OR inverse variance weighted [IVW] = 1.09, 95% CI = 1.05-1.13, P = 3.12×10 -6 for hypothyroidism; OR IVW = 1.08, 95% CI = 1.04-1.12, P = 8.14×10 -5 for hyperthyroidism). We found that FT4 levels were protective against lung cancer risk (OR IVW = 0.93, 95% CI = 0.87-0.99, P = 0.030). Additionally, the stratified MR analysis demonstrated the distinct causal effect of thyroid dysfunction on lung cancer risk among smokers. Hyperthyroidism mediated the effect of smoking behavior, especially the age of smoking initiation (17.66% mediated), on lung cancer risk. Thus, thyroid dysfunction phenotypes play causal roles in lung cancer development exclusively among smokers and act as mediators in the causal pathway from smoking to lung cancer.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-11"},"PeriodicalIF":2.2,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Hypothyroidism affects cholelithiasis causally: A two-sample bidirectional Mendelian randomization study. 甲状腺功能减退与胆石症有因果关系：一项双样本双向孟德尔随机研究。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.38.20240264

Xu Han, Hong Zhu

引用次数: 0

Chromosomal passenger complex-cyclin/CDK axis correlated with poor lung cancer prognosis. 染色体乘客复合体-细胞周期蛋白/CDK轴与肺癌预后不良相关

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.38.20240296

Prerna Vats, Sakshi Nirmal, Ashok Kumar, Rajeev Nema

引用次数: 0

Author Correction: CircPVT1 promotes silica-induced epithelial-mesenchymal transformation by modulating the miR-497-5p/TCF3 axis. 作者更正：CircPVT1通过调节miR-497-5p/TCF3轴促进二氧化硅诱导的上皮-间质转化。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2025-01-25 DOI: 10.7555/JBR.39.20250900

Siyun Zhou, Yan Li, Wenqing Sun, Dongyu Ma, Yi Liu, Demin Cheng, Guanru Li, Chunhui Ni

引用次数: 0

Author Correction: X-ray irradiation selectively kills thymocytes of different stages and impairs the maturation of donor-derived CD4 ⁺CD8 ⁺ thymocytes in recipient thymus. 作者更正：x射线照射选择性地杀死不同阶段的胸腺细胞，并损害受体胸腺中供体来源的CD4 +CD8 +胸腺细胞的成熟。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20249001

Jinbo Li, Hongquan Cai, Jianliang Jin, Qian Wang, Dengshun Miao

引用次数: 0

Intermediate filaments and their associated molecules. 中间细丝及其相关分子。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20240193

Jing Gao, Fumihiko Nakamura

引用次数: 0

Letter to the Editor The presence of glutathione S-transferase in recombinant S100A9 alters its effect on human sperm function. 重组S100A9中谷胱甘肽s转移酶的存在改变了其对人类精子功能的影响。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-12-25 DOI: 10.7555/JBR.38.20240155

Estefania Massa, Gastón Prez, Sergio Ghersevich

引用次数: 0

Hepatic SIRT6 protects against cholestatic liver disease primarily via inhibiting bile acid synthesis. 肝脏SIRT6主要通过抑制胆汁酸合成来预防胆汁淤积性肝病。

IF 2.2 4区医学

Journal of Biomedical Research Pub Date : 2024-11-25 DOI: 10.7555/JBR.38.20240172

Wen Zhang, Jiahui Wang, Luyao Yang, Yuyun Shao, Hongjun Peng, Longfeng Jiang, Liang Sheng

{"title":"Hepatic SIRT6 protects against cholestatic liver disease primarily via inhibiting bile acid synthesis.","authors":"Wen Zhang, Jiahui Wang, Luyao Yang, Yuyun Shao, Hongjun Peng, Longfeng Jiang, Liang Sheng","doi":"10.7555/JBR.38.20240172","DOIUrl":"https://doi.org/10.7555/JBR.38.20240172","url":null,"abstract":"Cholestatic liver disease, caused by the accumulation of hazardous bile acids in the liver, may result in cirrhosis, fibrosis, or liver failure. Activation of SIRT6 prevents cholestasis-associated pathological events, such as oxidative stress and mitochondrial biogenesis disorders, and inhibits bile acid synthesis to alleviate cholestatic liver injury. However, it is still uncertain which pathway is responsible for the therapeutic effect of SIRT6 in reducing cholestasis. Therefore, we treated liver-specific Sirt6 knockout mice with N-Acetylcysteine, Keap1-Nrf2-IN-1, or acadesine to remove oxidative stress and/or trigger mitochondrial biogenesis after cholestatic liver disease modeling, but these measures did not significantly improve cholestatic symptoms. However, MDL801, a SIRT6 agonist that downregulating CYP7A1, the key enzyme in bile acid synthesis, exhibited favorable therapeutic effects. In addition, the hepatic knockdown of Cyp7A1 further confirmed that inhibition of hepatic bile acid synthesis might be the main pathway by which SIRT6 alleviates cholestatic liver disease. These findings provide a solid basis for the potential application of SIRT6 agonists in the treatment of cholestatic liver disease.","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.2,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142769215","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0