María Rullan, Daniel Oyon, Javier Rández-Garbayo, Lucía Zabalza, Luis Carlos Saiz, Leire Leache, Marta Gutiérrez-Valencia, Matías A Ávila, Juan J Vila, Jesús M Urman
{"title":"Overall survival, clinical significance and biochemical composition of 'white bile' in patients with impaired biliary drainage: a systematic review.","authors":"María Rullan, Daniel Oyon, Javier Rández-Garbayo, Lucía Zabalza, Luis Carlos Saiz, Leire Leache, Marta Gutiérrez-Valencia, Matías A Ávila, Juan J Vila, Jesús M Urman","doi":"10.1007/s13105-026-01177-z","DOIUrl":"10.1007/s13105-026-01177-z","url":null,"abstract":"<p><p>White bile (WB) is a colourless and transparent watery fluid sometimes observed in the biliary system. The clinical significance and underlying mechanisms of this condition remain unclear. This systematic review evaluated overall survival (OS) between patients with WB and coloured bile (CB) and malignant biliary obstruction and described all available evidence regarding the prevalence, aetiology and composition of WB. We conducted a systematic search on PubMed, Scopus and Web of Science using the terms “white”, “translucent” and “clear bile” (February 28th, 2025). Data were independently screened and synthesized using a predefined data template considering the studies objectives and results. Overall survival was considered the main outcome. The quality of the studies was assessed using the Joanna Briggs Institute standardized critical appraisal tool. From 473 initial records, 31 studies with 302 patients with WB were included (5 cohort studies, 1 case-control study and 25 case reports or case series). Six studies investigated the prognostic significance of WB: three found association between WB and longer OS, one found association only in the non-operable group and two did not find it. The prevalence of WB varied from 2.9% to 53.4% and resulted from both malignant and benign conditions impairing biliary drainage. Bile levels of bilirubin, bile salts and cholesterol were practically absent in WB and serum bilirubin was higher when compared WB with CB. The association of WB with worse survival in patients with malignant biliary obstruction could not be established with the current evidence. To clarify its prognostic significance, further well-designed studies are needed.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147662504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Ziling Mai, Huijun Du, Yuhan Chen, Yaner Lu, Bingchen Liu, Deqiang Sun
{"title":"Identification of mitochondria-related genes in calcific aortic valve disease by integrated analysis of single-cell and bulk transcriptomic atlases.","authors":"Ziling Mai, Huijun Du, Yuhan Chen, Yaner Lu, Bingchen Liu, Deqiang Sun","doi":"10.1007/s13105-026-01176-0","DOIUrl":"10.1007/s13105-026-01176-0","url":null,"abstract":"<p><p>Calcific aortic valve disease (CAVD) is a highly prevalent heart valve disorder in which mitochondria act as critical regulators of calcification, yet their precise pathogenic mechanisms remain unclear. To elucidate these mechanisms, we integrated single-cell transcriptomic datasets comparing normal and calcified human aortic valves to identify 200 differentially expressed mitochondria-related genes (DE-MRGs), each exhibiting distinct expression patterns across diverse cellular subpopulations. Pseudotime trajectory analysis revealed 18 DE-MRGs with dynamic changes during the endothelial-to-mesenchymal transition, and intercellular communication analysis highlighted enhanced signaling between valve interstitial cells (VICs) and macrophages. Specifically, we hypothesized that distinct mitochondrial hubs may modulate these interactions. Using machine learning and bulk transcriptomic data, we identified microsomal glutathione S-transferase 1 (MGST1), an enzyme located on the outer mitochondrial and endoplasmic reticulum membranes, as a hub gene with high predictive performance. Subsequent validation confirmed that MGST1 is functionally involved in calcification, as its expression was markedly upregulated under calcifying conditions. Molecular docking further predicted that ritlecitinib exhibits the highest binding affinity for MGST1, and this molecule was shown to ameliorate calcification. In conclusion, this study delineates a comprehensive molecular network of MRGs in CAVD pathogenesis and identifies MGST1 as a mitochondria‑related hub gene that is upregulated in CAVD and functionally promotes calcification in vitro.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13068690/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147645791","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Francisco Mayo, Lourdes González-Vinceiro, Laura Hiraldo-González, Ismael Torres-Rubio, Claudia Calle-Castillejo, Elaheh Sobh-Doush, Reposo Ramírez-Lorca, Miriam Echevarría
{"title":"The postnatal expression of transcripts and proteins in the corpus callosum, as well as its myelinization, is affected by the congenital absence of AQP4.","authors":"Francisco Mayo, Lourdes González-Vinceiro, Laura Hiraldo-González, Ismael Torres-Rubio, Claudia Calle-Castillejo, Elaheh Sobh-Doush, Reposo Ramírez-Lorca, Miriam Echevarría","doi":"10.1007/s13105-026-01173-3","DOIUrl":"10.1007/s13105-026-01173-3","url":null,"abstract":"<p><p>During postnatal development in mice there is a marked switch in the expression of AQP4 from white to grey matter regions. A microglial population, CD11c+, which has been shown to be involved in normal postnatal development of the corpus callosum (CC), prolongs its expression in this tissue in the absence of AQP4. Here, we investigated the correlation between the levels of AQP4 expression during the early postnatal period and the expression of marker genes related to oligodendrogenesis in the mouse CC. A microarray transcriptomic analysis of the CC of wild-type (WT) and AQP4-KO (KO) mice was performed, validation of differentially expressed genes was done by RT-qPCR, and protein expression was analyzed by immunofluorescence. Overexpression of genes associated with microglia and astrocytes and inhibition of genes associated with mature oligodendrocytes were observed in the KO animal compared to the WT. GFAP and CD11c signals were significantly higher in the CC of the KO animal, as was the number of OPCs (OLIG2+/PDGFRa+). However, the number of mature oligodendrocytes (OLIG2+/CC1+) was reduced in the KO mice, indicating a failure of the oligodendrogenesis process that results in a significant reduction in the number of myelinated axons in the CC of the KO animal. This mouse model of congenital AQP4 deficiency, which shows defects in the maturation of its oligodendrocytes in the CC, provides insight into the role of AQP4 in demyelinating pathology and could help in the development of new diagnostic and/or therapeutic strategies for such diseases.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038659/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Victor Yassuda, Beatriz Sequeira, Ana Luísa De Sousa-Coelho
{"title":"The impact of bariatric and metabolic surgery on the levels of circulating growth differentiation factor 15 in humans.","authors":"Victor Yassuda, Beatriz Sequeira, Ana Luísa De Sousa-Coelho","doi":"10.1007/s13105-026-01160-8","DOIUrl":"10.1007/s13105-026-01160-8","url":null,"abstract":"<p><p>Obesity is a known risk factor cardiovascular disease, type 2 diabetes, metabolic dysfunction-associated steatotic liver disease (MASLD) and steatohepatitis (MASH), characterized by a state of chronic inflammation. In this stress context, many hepatokines and adipokines may be released, including Growth Differentiation Factor 15 (GDF15). GDF15 is involved in the regulation of appetite and metabolism, showing potential for the treatment of obesity and related comorbidities. This review aimed to evaluate the impact of bariatric and metabolic surgery (BMS) in the levels of circulating GDF15 in individuals with obesity. Considering the studies available, reporting GDF15 levels before and 12 months after BMS, the profile of GDF15 changes was not a consensus, and was not fully explained by differences in the characterization of the population in each study. This review also discusses the multiple sources of GDF15 in obesity and in response to its surgical treatment, where pathological, pharmacological, and behavioral factors may all be important contributors.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13038775/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581520","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Xiang Gao, Song Dai, Jiahao Li, Tao Wang, Xulong Sun, Pengzhou Li
{"title":"Odevixibat ameliorates high-fat diet-induced MASLD in mice by targeting the gut microbiota-metabolite axis and enhancing gut-liver crosstalk.","authors":"Xiang Gao, Song Dai, Jiahao Li, Tao Wang, Xulong Sun, Pengzhou Li","doi":"10.1007/s13105-026-01165-3","DOIUrl":"10.1007/s13105-026-01165-3","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent metabolic disorder with limited therapeutic options. This study aimed to investigate the therapeutic effects and underlying mechanisms of Bylvay (odevixibat) on high-fat diet (HFD)-induced MASLD in mice, focusing on liver pathology, gut barrier integrity, and the gut-liver axis via 16 S rRNA gene sequencing and untargeted metabolomics. Bylvay Odevixibat significantly ameliorated hepatic steatosis, inflammation, and liver injury markers. It restored gut barrier integrity, notably reversing HFD-induced dysbiosis, including Akkermansia and Desulfovibrio, and normalized key metabolites like LysoPC (20:5) and trichloroethanol glucuronide. Mechanistically, Bylvay treatment promoted the restructuring of the gut microbiota, which correlated with improved metabolic health. The abundance of trichloroethanol glucuronide was negatively correlated with Muribaculaceae and Lactobacillus abundance. The abundance of LysoPC (20:5(5Z,8Z,11Z,14Z,17Z)/0:0) exhibited a positive correlation with the abundance of Muribaculaceae, Alistipes, Lactobacillus, Alloprevotella and Desulfovibrio, and a negative correlation with Akkermansia and Bacteroides abundance. In summary, our findings reveal the therapeutic potential of Bylvay (odevixibat) in MASLD management, emphasizing the critical role of the interplay between gut microbiota, metabolites, and the gut-liver axis.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147581544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Gut microbiota-derived extracellular vesicles: novel perspectives from host-microbe interactions to therapeutic applications.","authors":"Yuwei Han, Yuying Guo, Wenzhe Xu, Yunsha Zhang, Hongying Hao, Yanhong Song, Nanjin Yu, Linna Zhao, Shixin Xu","doi":"10.1007/s13105-026-01175-1","DOIUrl":"10.1007/s13105-026-01175-1","url":null,"abstract":"<p><p>The gut microbiota plays a critical role in maintaining human health and is closely associated with the onset and progression of various diseases through its influence on immune regulation, metabolic homeostasis, intestinal barrier integrity, and the nervous system. In recent years, gut microbiota-derived extracellular vesicles(GMEVs) have attracted increasing attention as emerging mediators of host-microbe communication. These nanoscale vesicles possess a lipid bilayer membrane and are capable of encapsulating diverse bioactive molecules such as proteins, lipids, and nucleic acids. As essential mediators of intercellular communication, GMEVs act as molecular messengers that facilitate host–microbiota interactions. GMEVs exhibit high stability, excellent biocompatibility, and low immunogenicity, making them unlikely to trigger adverse immune reactions and thus promising candidates for clinical applications. Their ability to cross biological barriers further underscores their potential as vehicles for targeted drug delivery. This review provides a comprehensive overview of the physiological relevance of the gut microbiota and the biogenesis, molecular composition, and communication mechanisms of GMEVs. Special attention is given to the roles of GMEVs in the pathogenesis of inflammatory bowel disease (IBD), neurological disorders, and metabolic diseases. As ongoing research advances our understanding of the biological properties and disease-specific functions of GMEVs, these vesicles are emerging as novel therapeutic targets and strategic tools in precision medicine. Finally, this review discusses recent progress in GMEVs-based therapeutic strategies, offering new insights and possibilities for the treatment of diverse diseases.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147512851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wei-Hua Tan, Zheng-Liang Peng, Ting You, Zhi-Lu Sun
{"title":"Retraction Note: CTRP15 promotes macrophage cholesterol efflux and attenuates atherosclerosis by increasing the expression of ABCA1.","authors":"Wei-Hua Tan, Zheng-Liang Peng, Ting You, Zhi-Lu Sun","doi":"10.1007/s13105-026-01174-2","DOIUrl":"https://doi.org/10.1007/s13105-026-01174-2","url":null,"abstract":"","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147504180","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Azam Abedi, Mehrdad Moosazadeh Moghaddam, Reza Kachuei, Abbas Ali Imani Fooladi
{"title":"Exploring the role of metabolic disorders and gut microbiome in immune checkpoint regulation in cancer: PI3K/AKT/mTOR focus.","authors":"Azam Abedi, Mehrdad Moosazadeh Moghaddam, Reza Kachuei, Abbas Ali Imani Fooladi","doi":"10.1007/s13105-026-01171-5","DOIUrl":"10.1007/s13105-026-01171-5","url":null,"abstract":"<p><p>Metabolic disorders including obesity, hyperglycemia, and dyslipidemia contribute to cancer progression by overactivating signaling pathways, particularly PI3K/AKT/mTOR, thereby promoting tumor cell growth, survival, and migration. These metabolic disruptions also contribute to chronic inflammation, which leads to increased expression of immune checkpoint inhibitory proteins such as PD-L1 on immune and cancer cells, thereby suppressing the function of cytotoxic T cells within the tumor microenvironment. In parallel, gut microbiome dysbiosis characterized by a reduction in SCFA-producing bacteria and an increase in endotoxin-producing microbes results in increased intestinal epithelial permeability, allowing translocation of endotoxins into the bloodstream and activation of APCs. This process shifts the immune balance toward immunosuppressive cell populations and enhances the expression of inhibitory molecules such as PD-L1. This review focuses on the interplay of these factors and investigates the role of the gut microbiome in modulating the efficacy of immunotherapy, highlighting the impact of specific bacterial species in either enhancing or impairing the response to immune checkpoint inhibitors.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147490852","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Prognostic implications and molecular mechanisms of derived organoid-angiogenesis-related genes (DOARGs) in colorectal cancer.","authors":"Qian Xu, Mengli Dong, Ye Yuan, Qianqian Zhang","doi":"10.1007/s13105-026-01162-6","DOIUrl":"10.1007/s13105-026-01162-6","url":null,"abstract":"<p><p>This research seeks to investigate the prognostic significance and molecular mechanisms of derived organoid-angiogenesis-related genes (DOARGs) in colorectal cancer (CRC). DOARGs associated with CRC prognosis were screened based on The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases. Machine learning techniques were employed to create and assess a signature based on DOARGs, and a nomogram was constructed. Additionally, assessments were conducted on the levels of tumor mutational burden (TMB), immune infiltration, potential chemotherapeutic agents, and immune therapy responses to assess variations between groups with varying risk levels. In vitro experiments, including quantitative reverse-transcription polymerase chain reaction (qRT-PCR), Western blot, CCK-8, and transwell assays were conducted to verify the expression and molecular mechanisms of the model genes. A total of 13 DOARGs significantly associated with prognosis were identified. Five model genes (tissue inhibitor of metalloproteinases 1 (TIMP1), matrix metalloproteinase-1 (MMP1), C-C motif chemokine ligand 24 (CCL24), melanotransferrin (MELTF), and lymphoid enhancer-binding factor 1 (LEF1)) were identified for prognostic signature establishment. This signature demonstrated robust predictive performance for CRC prognosis upon validation. Significant differences were observed in TMB, immune infiltration, potential chemotherapeutic responses, and immune therapy reactions between groups with varying risk levels. Subgroup analysis categorized tumor samples into C1 and C2 groups, with C1 exhibiting significantly lower survival rates compared to C2. qRT-PCR analysis indicated a marked upregulation in the expression of the five model genes in CRC cells, and low expression of CCL24 suppressed the biological functions of CRC cells. This study has developed a prognostic signature for CRC utilizing DOARGs. This signature offers novel targets for the prognosis and personalized treatment of CRC.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147486442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}