Journal of Biomedical Research最新文献

{"title":"Bisphenol A impairs contractile function and vascular development in human cardiac organoids: Insights from toxicity assessment and evidence-based risk evaluation.","authors":"Linfeng Jiang, Yachang Wang, Huina Li, Yang Yang","doi":"10.7555/JBR.39.20250533","DOIUrl":"10.7555/JBR.39.20250533","url":null,"abstract":"<p><p>Bisphenol A (BPA), a widely encountered environmental endocrine-disrupting chemical, has been linked to an increased risk of congenital heart defects in epidemiological and experimental studies. To investigate its impact in a human-relevant system, we used a human cardiac organoid (hCO) model derived from human embryonic stem cells and exposed hCOs to BPA concentrations ranging from environmentally relevant to higher experimental levels (0.1-10 μmol/L) throughout differentiation. BPA exposure impaired cardiac contractile function and disrupted endothelial network formation, with more pronounced functional effects at higher concentrations. BPA exposure also induced apoptosis in hCOs. Subsequently, transcriptomic profiling revealed dysregulation of genes associated with cardiac rhythm and developmental signaling in BPA-treated hCOs. Among the concentrations tested, 0.5 μmol/L was the lowest concentration associated with a significant reduction in CD31 fluorescence intensity. This research provides <i>in vitro</i> evidence that BPA can perturb key processes in early human heart development, highlighting the necessity for further mechanistic and <i>in vivo</i> studies to clarify exposure relevance and its potential implications for fetal heart health.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"448-462"},"PeriodicalIF":3.7,"publicationDate":"2026-07-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13438319/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147573844","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":"Bronchial mucous gland adenoma: a rare case report and literature review.","authors":"Wang Wan, ZhuoHong Ye, GuoXiong Zeng, Heng Jiang, Biao Deng, XueFeng Wang, YanXia Wu, Zhu Liang","doi":"10.7555/JBR.39.20250534","DOIUrl":"https://doi.org/10.7555/JBR.39.20250534","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-7"},"PeriodicalIF":3.7,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678632","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}

{"title":"Low bone mineral density and handgrip strength are associated with increased risk of all-cause mortality: A cohort study with primary analysis and replication in 16,282 adults.","authors":"Xinyi Huang, Ningli Han, Kai Ling, Yu Liu, Qun Li, Ting Zhao, Jing Miao, Jinxin Cai, Jiahui Liu, Yao Fan, Chong Shen","doi":"10.7555/JBR.40.20260283","DOIUrl":"https://doi.org/10.7555/JBR.40.20260283","url":null,"abstract":"<p><p>This study aimed to evaluate the modifying effects and joint associations of handgrip strength (HGS) and bone mineral density (BMD) with all-cause mortality, with an exploratory analysis of cardiovascular disease (CVD) mortality. A primary analysis cohort ( <i>n</i> = 11150) and a replication cohort ( <i>n</i> = 5952) were included. Cox proportional hazards regression, restricted cubic spline analysis, and interaction analysis were used to examine the associations of BMD with mortality across relative HGS groups. Relative HGS was defined as absolute HGS divided by body weight. The joint effects of BMD-HGS combinations were assessed. During a median follow-up of 9.75 and 6.59 years, the primary analysis and replication cohorts recorded 1345 and 352 all-cause deaths, respectively. In the primary analysis cohort, low BMD was associated with an increased all-cause mortality risk in both the low and high relative HGS groups (hazard ratio [HR] = 1.26, 95% confidence interval [CI]: 1.04-1.52 and HR = 1.42, 95% CI: 1.16-1.74, respectively), with consistent findings in the replication cohort. No significant interaction was found between relative HGS and BMD ( <i>P</i> > 0.05). Participants with low BMD and low relative HGS had a 59%-62% higher risk of all-cause mortality than those with high BMD and high relative HGS in both cohorts, and the estimated PAR% for this combined exposure was 10.8%-13.1%. Results for CVD mortality were inconsistent across cohorts. In conclusion, low BMD with low handgrip strength is consistently associated with increased all-cause mortality, suggesting combined screening may benefit high-risk individuals.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-12"},"PeriodicalIF":3.7,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678682","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}

{"title":"DEC1 mediates IL-6-induced EMT in CRC <i>via</i> PI3K/AKT/NF-κB activation.","authors":"Enfang Shan, Weifeng Du, Ziheng Zhang, Jingwan Hu, Ying Huo, Wei Liu, Jian Yang","doi":"10.7555/JBR.39.20250440","DOIUrl":"https://doi.org/10.7555/JBR.39.20250440","url":null,"abstract":"<p><p>Colorectal cancer (CRC) represents a leading global malignancy. This study investigated the role of differentiated embryonic chondrocyte expressed gene 1 (DEC1) in interleukin-6 (IL-6)-induced invasion and migration of CRC. <i>In vitro</i>, IL-6 upregulated DEC1 expression and modulated the levels of epithelial-to-mesenchymal transition (EMT)-associated proteins in CRC cells. <i>DEC1</i> overexpression amplified the IL-6-induced invasion and migration phenotypes, increasing the expression of N-cadherin and vimentin but reducing E-cadherin expression. Conversely, <i>DEC1</i> knockdown attenuated these phenotypes, decreasing the expression of N-cadherin and vimentin but increasing E-cadherin expression. These findings suggest that IL-6 induced EMT through increasing DEC1. Moreover, <i>DEC1</i> overexpression increased the levels of basal and IL-6-stimulated phosphatidylinositol 3 kinase (PI3K) p110α, p-Akt, and p-p65, indicating activation of the PI3K/Akt/NF-κB signaling pathway. Conversely, <i>DEC1</i> knockdown diminished these effects. Notably, treatment with the inhibitor LY294002 or the NF-κB inhibitor EVP4593 significantly reversed the IL-6-induced upregulation of DEC1, the increase in N-cadherin and vimentin, and the reduction in E-cadherin. These <i>in vitro</i> findings were further corroborated <i>in vivo.</i> <i>Dec1</i> ^+/+ CRC mice exhibited elevated <i>Il6</i> mRNA levels and enhanced tumor invasion compared with <i>Dec1</i> ^-/- CRC mice. <i>Dec1</i> deficiency increased E-cadherin and decreased N-cadherin and vimentin, accompanied by inhibition of the PI3K/Akt/NF-κB signaling pathway in mice. Taken together, our results demonstrate that DEC1 mediates IL-6-induced invasion and migration of CRC <i>via</i> activation of the PI3K/Akt/NF-κB signaling pathway.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-14"},"PeriodicalIF":3.7,"publicationDate":"2026-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148678629","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}

{"title":"The immunological landscape of viral infections in asthma: mechanistic insights and therapeutic paradigm shifts.","authors":"Juntong Liu, Xinyue Han, Nan Lu, Yuhan Dou, Yuming Lu, Shuaijing Xie, Mingqi Lv, Guangyuan Zhang","doi":"10.7555/JBR.40.20260243","DOIUrl":"https://doi.org/10.7555/JBR.40.20260243","url":null,"abstract":"<p><p>Asthma is a common chronic respiratory disease in which respiratory viral infections-particularly rhinoviruses-are closely intertwined with disease manifestations. Such infections contribute substantially to pediatric asthma episodes and to a notable proportion of adult asthma presentations, reflecting the underlying immune dysregulation characteristic of asthma. Key components of the innate antiviral response-including the airway epithelium, dendritic cells, and natural killer cells-exhibit diminished antiviral activity in asthma, a deficiency that permits greater viral replication and persistence. Concurrently, individuals with asthma frequently exhibit type 2 immunity, an immune profile that drives IgE production, eosinophilic inflammation, and airway hyperresponsiveness. Children are particularly susceptible to the immunological impacts of respiratory viral infections in the context of asthma, potentially due to immune immaturity and less robust early-life antiviral defenses. Crucially, the crosstalk between innate and adaptive immunity dictates the severity of asthma-related clinical manifestations during viral infections: a compromised antiviral innate response, when paired with a type 2-skewed adaptive immune environment, can synergistically promote severe airway inflammation and airflow obstruction. Although inhaled corticosteroids (ICS) remain a cornerstone of maintenance therapy for preventing asthma exacerbations, ICS-based therapy does not fully prevent virus-associated exacerbations, particularly in patients with type 2-low, neutrophil-predominant, or severe uncontrolled asthma. By contrast, oral or systemic corticosteroids remain the first-line treatment for acute exacerbations, highlighting the need to distinguish maintenance ICS therapy from acute systemic corticosteroid use. Future therapeutic strategies should therefore prioritize enhancing antiviral immune responses and modulating virus-induced neutrophilic inflammation to better prevent and mitigate asthma-related clinical challenges associated with viral infections.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-26"},"PeriodicalIF":3.7,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390499","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}

{"title":"Cardiac xenotransplantation: Progress, barriers, and pathways toward clinical translation.","authors":"Shangxuan Li, Yi Wang, Dongsheng He, Jiahong Wang, Zekai Yu, Lu Yin, Ziqiang Dai, Zhipeng Ren, Guanzheng Cui, Xianzhi Wang, Gen Zhang, Huan Wang, Xin Li, Dianyuan Li","doi":"10.7555/JBR.40.20260177","DOIUrl":"10.7555/JBR.40.20260177","url":null,"abstract":"<p><p>Cardiac xenotransplantation (CXTx) has emerged as a potentially transformative solution to the global shortage of donor organs, driven by recent breakthroughs in genome-editing technologies. This review provides a comprehensive overview of the field, tracing its evolution from early experimental barriers to the current stage of early clinical translation. We summarize the significant strides made in the development of genetically engineered donor pigs, in which multi-gene modifications have effectively overcome the obstacle of hyperacute rejection. Despite these advances, long-term graft survival remains limited by complex immunological and physiological challenges, including acute humoral xenograft rejection, cellular immune responses, and coagulation dysregulation. Furthermore, this review critically analyzes data from recent milestones, including studies in brain-dead decedent models and the first genetically modified pig-to-human heart transplants. These clinical endeavors have exposed critical unresolved issues, particularly antibody-mediated rejection and the biosafety risks associated with porcine viruses. In conclusion, we discuss the key pathways for future progress, emphasizing the urgent need for optimized immunosuppressive regimens, rigorous viral surveillance, and standardized preclinical protocols to establish CXTx as a safe and durable clinical reality.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-20"},"PeriodicalIF":3.7,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148329664","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}

{"title":"<i>Helicobacter pylori</i>-induced <i>ADAMDEC1</i> overexpression in M2 macrophages drives preneoplastic progression in the gastric mucosa.","authors":"Haoxuan Kan, Guoyang Niu, Luyao Wang, Yifan Zou, Zihan Wan, Yihan Xu, Haojun Yang, Bowen Li, Zekuan Xu","doi":"10.7555/JBR.40.20260097","DOIUrl":"https://doi.org/10.7555/JBR.40.20260097","url":null,"abstract":"<p><p><i>Helicobacter pylori</i> ( <i>H. pylori</i>) infection is a major risk factor for gastric cancer, though the immune microenvironmental factors driving preneoplastic transformation remain unclear. In this study, single-cell RNA sequencing was used to characterize macrophage subsets and identify key genes associated with <i>H. pylori</i>-induced gastric lesions. Molecular, cellular, and <i>in vivo</i> assays were conducted to determine the mechanisms regulating the expression of a disintegrin and metalloproteinase-like decysin 1 ( <i>ADAMDEC1</i>) and its downstream effects. M2 macrophages were significantly enriched in <i>H. pylori</i>-positive gastritis and metaplasia, and <i>ADAMDEC1</i> showed progressive increase in expression during lesion progression. <i>H. pylori</i> promoted M2 polarization and induced <i>ADAMDEC1</i> transcription <i>via</i> signal transducer and activator of transcription 3 (STAT3) binding to its promoter. Functionally, M2-derived ADAMDEC1 increased soluble epidermal growth factor levels, thereby activating the epidermal growth factor receptor (EGFR)-extracellular signal-regulated kinase 1/2 (ERK1/2) signaling pathway in epithelial cells, which led to upregulation of C-C motif chemokine ligand 20 (CCL20) expression, enhanced proliferation, and impaired genomic stability. The present study reveals a potential <i>H. pylori</i>-driven oncogenic pathway involving the M2 macrophage-ADAMDEC1-EGF/EGFR/ERK axis, establishing ADAMDEC1 as a potential target for early intervention in <i>H. pylori</i>-associated gastric cancer.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-20"},"PeriodicalIF":2.4,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030670","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}

{"title":"Cardiomyocyte BMAL1 deficiency worsens obesity-related cardiomyopathy with heightened PINK1/Parkin-linked mitophagy and mitochondrial dysfunction.","authors":"Tianzi Liu, Xiaoxuan Fan, Nannan Zhang, Yao Wang, Zhiyong Qian, Xiaofeng Hou, Hanwen Zhang, Jiangang Zou","doi":"10.7555/JBR.40.20260012","DOIUrl":"https://doi.org/10.7555/JBR.40.20260012","url":null,"abstract":"<p><p>Obesity-related cardiomyopathy (OCM) is characterized by pathological cardiac remodeling and progressive functional decline, often accompanied by mitochondrial dysfunction, particularly aberrant mitophagy. The role of the core circadian gene brain and muscle ARNT-like protein 1 ( <i>Bmal1</i>) in OCM remains unclear. In this study, we employed a high-fat diet (HFD)-induced OCM mouse model, a cardiomyocyte-specific <i>Bmal1</i> knockout ( <i>Bmal1</i> ^CMKO) model, and a palmitic acid (PA)-induced H9c2 cardiomyocyte injury model to investigate the function of <i>Bmal1</i>. <i>In vivo</i>, BMAL1 expression was reduced in hearts of HFD mice; HFD- <i>Bmal1</i> ^CMKO mice exhibited exacerbated myocardial hypertrophy, fibrosis, functional impairment, and apoptosis, accompanied by increased expression of the mitophagy-related proteins PINK1, Parkin, and LC3-II. <i>In vitro</i>, PA exposure decreased BMAL1 expression, disrupted mitochondrial membrane potential, increased reactive oxygen species generation, and induced excessive mitophagy; these effects were aggravated by <i>Bmal1</i> silencing and attenuated by <i>Bmal1</i> overexpression, which also improved cell viability. Collectively, these findings indicate that <i>Bmal1</i> plays a protective role in OCM, and its downregulation may be a key contributor to obesity-induced cardiac remodeling and dysfunction. Mechanistically, BMAL1 downregulation was accompanied by activation of the PINK1/Parkin signaling and enhanced mitophagy under lipid stress. By restraining excessive mitophagy and preserving mitochondrial function and metabolic homeostasis, <i>Bmal1</i> and its associated pathways may represent promising therapeutic targets for OCM.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.4,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148015767","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}

{"title":"Surface electromyography for evaluating the impact of focused ultrasound on the sciatic nerve modulation in rats.","authors":"Zongqi Tu, Xingchao Wang, Yufeng Zhou","doi":"10.7555/JBR.40.20260049","DOIUrl":"https://doi.org/10.7555/JBR.40.20260049","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-7"},"PeriodicalIF":2.4,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148211341","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}

{"title":"<i>Lactobacillus murinus</i> improves liver fibrosis in primary sclerosing cholangitis mice by decreasing taurocholic acid and regulating M2 macrophage polarization.","authors":"Chenchen Zhang, Zixuan Wang, Dilixiati Kadier, Yu Shen, Zejia Hao, Yutong Zhu, Qian Wu, Lei Li, Ping Jiang","doi":"10.7555/JBR.40.20260064","DOIUrl":"https://doi.org/10.7555/JBR.40.20260064","url":null,"abstract":"<p><p>Hepatic accumulation of bile acids (BAs) contributes to cholestasis-induced liver injury and fibrosis. Our previous studies have shown that <i>Lactobacillus murinus</i> ( <i>L. murinus</i>) alleviates liver fibrosis in primary sclerosing cholangitis (PSC) by modulating bile acid metabolism. In this study, we found that <i>L. murinus</i> intervention alleviated hepatic taurocholic acid (TCA) accumulation, cholestasis, and liver fibrosis in PSC mice. TCA was shown to promote liver fibrosis in PSC mice by enhancing M2 macrophage-mediated secretion of transforming growth factor beta 1 (TGF-β1). Macrophage depletion in PSC mice reduced the proportion of M2 macrophages and TGF-β1 cytokine levels, alleviating liver fibrosis. <i>L. murinus</i> exhibited bile salt hydrolase (BSH) activity, preferentially hydrolyzing glycine-conjugated bile acids. Furthermore, <i>L. murinus</i> reduced TCA reabsorption into the portal circulation by suppressing farnesoid X receptor ( <i>Fxr</i>) gene expression in the ileum, thereby alleviating hepatic TCA accumulation and mitigating liver fibrosis in PSC mice. These findings suggest that <i>L. murinus</i> mitigates PSC-associated liver fibrosis, which is associated with reduced TCA levels and regulation of M2 macrophage polarization, offering a potential therapeutic strategy for PSC.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":2.4,"publicationDate":"2026-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148015705","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}