Journal of Biomedical Research最新文献

{"title":"Taxonomic diversity of fecal microbiota associated with different metabolic phenotypes in residents of Arkhangelsk, Northwestern Russia.","authors":"Anna Postoeva, Ekaterina Krieger, Anna Leontyeva, Alexander V Kudryavtsev, Julia Galeeva, Dmitry Fedorov, Polina Kuzmichenko, Elena Ilina, Vadim Govorun","doi":"10.7555/JBR.39.20250258","DOIUrl":"10.7555/JBR.39.20250258","url":null,"abstract":"<p><p>The study aimed to assess the taxonomic diversity and composition of gut microbiota in Arkhangelsk residents, Northwestern Russia, with varying metabolic statuses. A population-based cross-sectional \"Know Your Heart\" study (2015-2017, participants aged 35-69 years) included a health examination and gut microbiota analysis ( <i>n</i> = 685). Participants were divided into four metabolic phenotypes: metabolically healthy non-obese (MHN), metabolically unhealthy non-obese (MUN), metabolically healthy obese (MHO), and metabolically unhealthy obese (MUO). Analyses were performed using RStudio software (v.4.2.0) with the vegan and phyloseq packages (v.1.42.0) for microbiota analysis. The sample was distributed across phenotypes as follows: MHN (47.6%), MUN (22.1%), MHO (10.4%), and MUO (19.9%). Beta-diversity analysis revealed significant differences in overall microbiome composition between MUO and MHN participants, while alpha-diversity did not differ significantly across phenotypes. The MHN group was characterized by a higher abundance of beneficial commensals such as <i>Christensenellaceae R-7</i> group, <i>Ruminococcaceae UCG-005</i>, and <i>Eubacterium xylanophilum</i> group, which are taxa previously associated with metabolic health and longevity. In contrast, the MUO group showed an increased abundance of <i>Streptococcus salivarius</i> and <i>Negativibacillus</i>, taxa linked to gut dysbiosis and metabolic disorders. <i>Blautia spp</i>. emerged as a major hub in the microbiota of obese participants, consistent with its reported association with visceral fat. In conclusion, microbial composition was similar in obese participants despite metabolic dysfunction, whereas unidirectional taxonomic shifts were observed in those with metabolic dysfunction alone. The differences in the predominance of microbial taxa across metabolic phenotypes suggest that these taxa have a role in the development of metabolic disorders and obesity.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":3.7,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145458596","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 crosstalk between autophagy and ferroptosis in pulmonary fibrosis.","authors":"Rongzhu Liu, Dongnan Zheng, Fengxu Wang, Mengna Jiang, Rui Zhao, Shan Bao, Xinyuan Zhao, Demin Cheng","doi":"10.7555/JBR.39.20250243","DOIUrl":"10.7555/JBR.39.20250243","url":null,"abstract":"<p><p>Pulmonary fibrosis (PF) is a progressive lung disorder characterized by excessive deposition of extracellular matrix (ECM) in the alveoli, with irreversible fibrotic remodeling and destruction of alveolar structures. Clinically, PF is manifested by progressive dyspnea and a decline in lung function. These manifestations contribute to a poor prognosis and significantly diminish the quality of life of affected individuals. Current therapeutic options for PF remain limited, highlighting the urgent need to elucidate its molecular mechanisms in order to develop novel treatment strategies. Recent studies have revealed that autophagy and ferroptosis, two critical cell death pathways, engage in intricate crosstalk mechanisms that regulate the pathogenesis of PF. Autophagy maintains cellular homeostasis by mediating lysosome-dependent degradation, whereas ferroptosis is characterized by iron-dependent lipid peroxidation. The interplay between autophagy and ferroptosis plays a pivotal role in modulating fibrosis progression. However, the mechanistic interactions between autophagy and ferroptosis in PF remain poorly understood, particularly regarding their bidirectional crosstalk and their unique role in PF progression. This review aims to systematically synthesize the current understanding of autophagy-ferroptosis interactions in PF, thereby identifying potential therapeutic strategies and drug targets for PF treatment.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-17"},"PeriodicalIF":3.7,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13620458/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145345440","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":"Editorial commentary on the special issue of cancer research.","authors":"","doi":"10.7555/JBR.39.20250800","DOIUrl":"10.7555/JBR.39.20250800","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":"39 5","pages":"439-440"},"PeriodicalIF":3.7,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481670/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145191584","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 mediating effect of blood pressure between healthy lifestyles and stroke: Results from the China Kadoorie Biobank study.","authors":"Zidong Wang, Jiaxi Zhou, Xikang Fan, Jian Su, Houyue Geng, Xun Wu, Yujie Hua, Hongfu Ren, Jun Lyu, Pei Pei, Canqing Yu, Dianjianyi Sun, Yan Lu, Jinyi Zhou, Ran Tao","doi":"10.7555/JBR.39.20250177","DOIUrl":"10.7555/JBR.39.20250177","url":null,"abstract":"<p><p>While a healthy lifestyle is known to reduce the risk of stroke, the extent to which blood pressure (BP) mediates this association remains unclear. The present study aimed to quantify the mediating role of BP in the association between combined lifestyle factors and stroke incidence. Using data from 51929 participants free of major cardiovascular diseases or cancer at baseline, we employed structural equation modeling to assess the mediating effects of systolic (SBP) and diastolic (DBP) blood pressure. During the follow-up, 2811 incident stroke cases were identified. A healthy lifestyle was significantly associated with a reduced risk of stroke, with SBP mediating 44.70% ( <i>β</i> = -0.0014, 95% confidence interval [CI]: -0.0016 to -0.0012) and DBP mediating 37.81% ( <i>β</i> = -0.0012, 95% CI: -0.0015 to -0.0009) of this association. The mediating effects were attenuated but remained significant for ischemic stroke (SBP: 33.21%; DBP: 27.24%). In conclusion, approximately two-fifths of the protective association between a healthy lifestyle and stroke may be mediated by BP. These findings suggest that BP control may serve as an important early indicator for evaluating the effectiveness of lifestyle interventions in reducing stroke risk.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"23-31"},"PeriodicalIF":2.4,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12799335/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144955261","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":"HDGF derived from Müller cells enhances the activation of microglia in diabetic retinopathy.","authors":"Aowang Qiu, Wenjie Yin, Ningyu Wang, Xin Wang, Qinghuai Liu, Weiwei Zhang","doi":"10.7555/JBR.38.20240386","DOIUrl":"10.7555/JBR.38.20240386","url":null,"abstract":"<p><p>Diabetic retinopathy (DR), a common complication of diabetes, is characterized by retinal angiogenesis and inflammation. The role of hepatoma-derived growth factor (HDGF) in mediating inflammation during DR remains unclear. We measured HDGF levels in the aqueous humor and found that HDGF was increased in DR but decreased after anti-angiogenesis treatment. Using public single-cell RNA sequencing datasets, we found that elevated HDGF in DR was mainly produced by Müller cells and targeted microglia. Additionally, integrin beta 2 ( <i>Itgb2</i>), a target gene of HDGF that induces microglial activation, was significantly upregulated in DR. To verify these results, we performed enzyme-linked immunosorbent assays, quantitative reverse transcription-PCR, Western blotting, and fluorescence immunostaining in cultured Müller and microglial cells treated with HDGF or anti-HDGF, as well as in DR mice receiving intravitreal injections of HDGF or its antibody. Exogenous HDGF further promoted microglial activation, migration, and secretion of pro-inflammatory cytokines, while neutralization of HDGF suppressed these effects caused by high glucose. Furthermore, the HDGF receptor nucleolin was overexpressed in microglia under high glucose stimulation. Therefore, blocking HDGF from Müller cells in DR reduced the excessive inflammatory response in microglia, highlighting HDGF as a potential therapeutic target.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"63-75"},"PeriodicalIF":2.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12794185/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794535","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":"Association between psoriasis and colorectal cancer: A meta-analysis.","authors":"Yufei Wang, Jiliang Lu, Ziyue Diao, Zhiqiang Yin","doi":"10.7555/JBR.39.20250175","DOIUrl":"10.7555/JBR.39.20250175","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"93-96"},"PeriodicalIF":2.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12794175/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649564","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":"Effect of overweight and obesity on serum interleukin-6 in children and adolescents with bronchial asthma.","authors":"Regina Niyazovna Khramova, Tatyana Ivanovna Eliseeva, Dmitriy Yuryevich Ovsyannikov, Maksim Aleksandrovich Karpenko, Elena Valerjevna Tush, Svetlana Viktorovna Krasilnikova, Daniil Vitalievich Azarnov, Sofya Alekseevna Teremova, Nailya Iskhakovna Kubysheva, Оlga Vladimirovna Khaletskaya, Natalia Anatolievna Geppe","doi":"10.7555/JBR.38.20240381","DOIUrl":"10.7555/JBR.38.20240381","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"1-3"},"PeriodicalIF":2.4,"publicationDate":"2025-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12683504/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690363","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":"Author correction: Association between exposure to particulate matter during pregnancy and birthweight: A systematic review and a meta-analysis of birth cohort studies.","authors":"Yinwen Ji, Fei Song, Bo Xu, Yining Zhu, Chuncheng Lu, Yankai Xia","doi":"10.7555/JBR.38.20240383","DOIUrl":"10.7555/JBR.38.20240383","url":null,"abstract":"<p><p>The effect of prenatal exposure to ambient particulate matter (PM) on birth weight varies considerably across studies, and the findings remain inconclusive. In this study, we conducted a meta-analysis to assess the associations between exposure to PM _2.5 and PM ₁₀ and birth weight. A total of 74 studies were identified through searches in Web of Science, PubMed, Embase, and Ovid Medline, as well as manual searches, up to October 2024. We found that for each 10 μg/m³ increase in PM _2.5, the risk of low birth weight (LBW) increased significantly during the entire pregnancy (odds ratio [OR] = 2.41, 95% confidence interval [CI]: 1.99-2.91) and in all trimesters. Similarly, for every 10 μg/m³ increase in PM ₁₀ concentration, the risk of LBW increased significantly during the entire pregnancy (OR = 1.46, 95% CI: 1.16-1.84). Subgroup analysis by maternal age for PM _2.5 showed that mothers aged 30 and above had a significantly higher risk of LBW (OR = 3.69, 95% CI: 2.81-4.84), compared with those under 30. In conclusion, maternal exposure to PM _2.5 and PM ₁₀ is associated with an increased risk of LBW across all trimesters. Additionally, mothers aged 30 and above are at a higher risk of LBW, compared with younger mothers. Further research is needed to clarify the biological mechanisms by which PM pollution may contribute to LBW.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"538-548"},"PeriodicalIF":2.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649565","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":"Long non-coding RNA <i>TUG1</i> regulates multiple glycolytic enzymes in hepatocellular carcinoma cells by sponging microRNA-122-5p.","authors":"Thammachanok Boonto, Chinnatam Phetkong, Chaiyaboot Ariyachet","doi":"10.7555/JBR.39.20250056","DOIUrl":"10.7555/JBR.39.20250056","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) remains the third leading cause of cancer-related deaths worldwide; however, its therapeutic options are limited. Understanding the molecular mechanisms of HCC could provide insight into new therapies. Emerging studies indicate the important role of long-noncoding RNAs (lncRNAs) in the pathogenesis of HCC. The expression of the well-studied lncRNA taurine upregulated gene 1 ( <i>TUG1</i>) is upregulated in HCC tissues, but its transcriptomic effects in HCC cells remain unexplored. We established <i>TUG1</i>-knockdown and control HCC cells for RNA-seq experiments. KEGG analysis revealed glycolysis as the top enriched pathway upon <i>TUG1</i> silencing. Accordingly, <i>TUG1</i>-depleted HCC cells showed impairments in glucose uptake, ATP synthesis, and lactate production. Clinical HCC tissue data revealed positive gene expression correlations between <i>TUG1</i> and several glycolysis-related genes. To identify a molecular function of <i>TUG1</i> in glycolysis, we explored the competing endogenous model and used bioinformatic tools to find the five microRNAs (miRNAs) that had the most binding sites for <i>TUG1</i>. Among these miRNAs, miR-122-5p exhibited an inverse correlation in gene expression with most <i>TUG1</i>-regulated glycolysis genes, including <i>PKM</i>, <i>ALDOA</i>, <i>ENO2</i>, and <i>PFKM</i>. Dual-luciferase assays demonstrated the direct interaction between <i>TUG1</i> and miR-122-5p and between miR-122-5p and the 3' untranslated regions of both <i>PKM</i> and <i>ALDOA</i>. We further showed that inhibition of miR-122-5p alleviated the suppression of glycolysis induced by <i>TUG1</i> depletion. Together, our RNA-seq analysis of <i>TUG1</i>-depleted HCC cells, combined with clinical data, reveals a critical role of <i>TUG1</i> in regulating glycolysis and provides new insight into its oncogenic function in HCC.</p>","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"515-529"},"PeriodicalIF":2.4,"publicationDate":"2025-07-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481678/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144690374","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 serum fascin-1 and tumor components containing this protein in patients with head and neck squamous cell carcinoma: A pilot study.","authors":"Gelena V Kakurina, Elena E Sereda, Marina N Stakheeva, Irina V Kondakova, Evgeny L Choinzonov","doi":"10.7555/JBR.38.20240397","DOIUrl":"10.7555/JBR.38.20240397","url":null,"abstract":"","PeriodicalId":15061,"journal":{"name":"Journal of Biomedical Research","volume":" ","pages":"534-537"},"PeriodicalIF":2.4,"publicationDate":"2025-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12481671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144649566","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}