Jonathan Robert Belanich, Tuomas Oskari Kilpeläinen
{"title":"Dual perspectives on human gene networks from gain- and loss-of-function interaction maps.","authors":"Jonathan Robert Belanich, Tuomas Oskari Kilpeläinen","doi":"10.1152/physiolgenomics.00023.2026","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00023.2026","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147857001","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Elaheh Rahbar, Jillian R Richter, Jessica C Cardenas
{"title":"Multiomic changes post-hypovolemia in a lower body negative pressure model: unlocking new mechanisms or adding to the complexity?","authors":"Elaheh Rahbar, Jillian R Richter, Jessica C Cardenas","doi":"10.1152/physiolgenomics.00042.2026","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00042.2026","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841671","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Physiological genomicsPub Date : 2026-05-01Epub Date: 2026-03-28DOI: 10.1152/physiolgenomics.00310.2025
Neil A Bradbury
{"title":"Beyond the lungs: what CF sheep reveal about liver disease in cystic fibrosis.","authors":"Neil A Bradbury","doi":"10.1152/physiolgenomics.00310.2025","DOIUrl":"10.1152/physiolgenomics.00310.2025","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":"213-215"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575200","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Publisher's note for Bhargava et al., volume 57, 2025, p. 343-356.","authors":"","doi":"10.1152/physiolgenomics.00110.2026_NOT","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00110.2026_NOT","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":"58 5","pages":"242"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147841721","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Physiological genomicsPub Date : 2026-05-01Epub Date: 2026-04-16DOI: 10.1152/physiolgenomics.00105.2026
Endin Nokik Stujanna, Jun Yoshioka
{"title":"NR4A2-driven metabolic reprogramming in the heart: from adaptive response to maladaptive remodeling.","authors":"Endin Nokik Stujanna, Jun Yoshioka","doi":"10.1152/physiolgenomics.00105.2026","DOIUrl":"10.1152/physiolgenomics.00105.2026","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":"239-241"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699501","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Physiological genomicsPub Date : 2026-05-01Epub Date: 2026-04-01DOI: 10.1152/physiolgenomics.00226.2025
Kyrah L Turner, Taylor G Christopherson, Bertrand C W Tanner
{"title":"Early fibrotic gene activation precedes structural remodeling in the heart of cardiac myosin binding protein-C knockout mice.","authors":"Kyrah L Turner, Taylor G Christopherson, Bertrand C W Tanner","doi":"10.1152/physiolgenomics.00226.2025","DOIUrl":"10.1152/physiolgenomics.00226.2025","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is the leading genetic cause of heart disease. Although research has been focused on HCM for the past several decades, clinical treatments for patients remain limited. The heart comprises several myofilament proteins that work together to facilitate proper contraction and relaxation to pump blood throughout the body. Cardiac myosin binding protein-C (cMyBP-C) is a thick-filament regulatory protein, and mutations in cMyBP-C are frequently linked with clinical cases of HCM. To further understand the role of cMyBP-C and its contribution to cardiac disease, we assessed the progressive development of molecular and morphological biomarkers associated with HCM in a cMyBP-C knockout mouse model. We assessed gene expression associated with hypertrophy, fibrosis, and sarcomeric proteins at 21, 60, and 183 days of age via a custom NanoString nCounter gene panel designed from clinically relevant human cardiac disease panels. Cardiac morphology and tissue remodeling were evaluated using biochemical and histological assays. Our findings unveil significant dysregulation in genes associated with hypertrophy and fibrosis in cMyBP-C deficient mice at 21 days old, which precedes irreversible overt fibrosis in the cardiac tissue. However, changes in sarcomeric gene expression only appeared after hypertrophy and fibrosis were established. The early changes in gene expression underscore the need for better understanding the mechanisms driving HCM development, which may offer potential avenues for therapeutic intervention before pathological remodeling occurs. Pharmaceutical interventions that target cardiac dysfunction may be most effective before cardiac remodeling, highlighting the potential utility for early screening and preventative strategies to manage genetic-based cardiomyopathies.<b>NEW & NOTEWORTHY</b> The effect of cMyBP-C ablation in the cardiac sarcomere induces cell-signaling changes that precede significant overt fibrosis. These data indicate that early clinical screening may allow for treatment before irreversible, pathological remodeling of the heart takes place.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":"216-224"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593861","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Physiological genomicsPub Date : 2026-05-01Epub Date: 2026-03-28DOI: 10.1152/physiolgenomics.00269.2025
Hari Naga Sai Kiran Suryadevara, R Caitlin Hebert, Jaroslaw Staszkiewicz, Eric Ravussin, Kara L Marlatt, Prachi Singh, Sujoy Ghosh
{"title":"Transcriptional remodeling of human skeletal muscle following sleep restriction in postmenopausal women.","authors":"Hari Naga Sai Kiran Suryadevara, R Caitlin Hebert, Jaroslaw Staszkiewicz, Eric Ravussin, Kara L Marlatt, Prachi Singh, Sujoy Ghosh","doi":"10.1152/physiolgenomics.00269.2025","DOIUrl":"10.1152/physiolgenomics.00269.2025","url":null,"abstract":"<p><p>Sleep is a critical regulator of metabolic health, but its impact on skeletal muscle remains underexplored. Given the muscle's pivotal role in glucose metabolism, energy homeostasis, and immune signaling, understanding how insufficient sleep affects global transcriptomic responses in skeletal muscle is of significant interest. In a randomized crossover design, skeletal muscle biopsies were collected from healthy postmenopausal women following four nights of habitual or restricted sleep (40% reduction). RNA-seq was performed on seven paired samples and analyzed using differential expression (DE), gene correlation, pathway enrichment, and transcription factor motif analysis. Global DE analysis revealed modest transcriptomic shifts, with nine genes consistently altered across multiple DE methods. Gene set enrichment analysis showed upregulation of oxidative phosphorylation and myogenesis pathways and downregulation of immune and inflammatory signaling during sleep restriction. Differential correlation analysis identified substantial reorganization in gene coexpression networks, particularly within RNA degradation and ribosomal pathways. Transcription factor and motif analyses suggested Yin Yang (YY1) as a possible key mediator of transcriptional reprogramming during sleep restriction. Motif analysis confirmed enrichment of <i>YY1</i> binding sites among differentially correlated genes, further implicating its role in linking circadian disruption, metabolic stress, and immune modulation. Sleep restriction for four nights triggers subtle but biologically meaningful changes in skeletal muscle transcriptomes. The simultaneous upregulation of mitochondrial and structural genes, alongside downregulation of immune-related genes, reflects a complex adaptive response. YY1 appears to be a central regulatory node linking sleep loss to muscle dysfunction, with implications for metabolic resilience, inflammation, and tissue repair.<b>NEW & NOTEWORTHY</b> Sleep restriction triggers coordinated transcriptional remodeling in postmenopausal women, including upregulated oxidative phosphorylation and myogenesis pathways, while suppressing immune and inflammatory signaling. Differential correlation analysis revealed substantial reorganization of gene coexpression networks. Transcription factor YY1 emerged as a key mediator linking sleep loss to metabolic and immune dysregulation in muscle. These findings reveal skeletal muscle's adaptive response to insufficient sleep and identify YY1 as a potential therapeutic target for sleep-related metabolic dysfunction.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":"225-238"},"PeriodicalIF":2.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13131446/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147575213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Emmanuel Dugrenot, Jérémy Orsat, Emmanuel Gouin, François Guerrero, Anthony Guernec
{"title":"Changes in Liver and Lung antioxidant and mitochondrial biogenesis gene expression in Decompression Sickness resistant rats.","authors":"Emmanuel Dugrenot, Jérémy Orsat, Emmanuel Gouin, François Guerrero, Anthony Guernec","doi":"10.1152/physiolgenomics.00218.2025","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00218.2025","url":null,"abstract":"<p><p>Susceptibility to decompression sickness (DCS) shows wide interindividual variability, the origins of which remain poorly understood. To better elucidate its mechanisms, we previously developed a rat strain with more than threefold higher resistance to DCS through selective breeding. In this study, we examined baseline expression of genes related to antioxidant defense and mitochondrial biogenesis in the lungs and liver of DCS-resistant and non-resistant Wistar rats. None of the animals were exposed to hyperbaric conditions, allowing us to focus on constitutive expression differences potentially underlying genetic resistance to DCS. Quantitative reverse transcription polymerase chain reaction (RT-qPCR) was performed, and data were analyzed using two-way ANOVA to assess the effects of selection, sex, and their interaction. In the lungs, no significant selection effect was observed for genes involved in mitochondrial biogenesis (<i>Pgc1α, Nrf1, Nrf2</i>) or antioxidant defense (<i>Sod1, Sod2, Gpx1,</i> and <i>Cat</i>). In contrast, in the liver, expression of both gene groups was significantly decreased in resistant rats (p < 0.0083, Bonferroni correction), except for <i>Pgc1α</i>. These lower hepatic expression levels align with the previously reported reduction in citrate synthase activity and lower basal oxygen consumption in the soleus muscle of resistant rats. Together, these findings suggest that hepatic metabolism and mitochondrial function may play key roles in DCS susceptibility, potentially through reduced mitochondrial activity and lower reactive oxygen species (ROS) production in resistant animals.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147778633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kun Huang, Shuo Zhang, Jinshuang Liu, Chengcheng Yang, Guangchun Zeng, Bo Li
{"title":"Pulmonary microbiota, local inflammation, and tumor progression impact immune checkpoint gene profiles in the lung microenvironment.","authors":"Kun Huang, Shuo Zhang, Jinshuang Liu, Chengcheng Yang, Guangchun Zeng, Bo Li","doi":"10.1152/physiolgenomics.00300.2025","DOIUrl":"https://doi.org/10.1152/physiolgenomics.00300.2025","url":null,"abstract":"<p><p>Emerging data indicates that the lung microbiota contribute to the initiation and progression of lung cancer. Here, we investigate a wide range of immune checkpoint genes (ICGs) in the pulmonary microenvironment across lung carcinogenesis and explore the interplay between these immunoregulatory genes, the intratumoral microbiota, and inflammatory processes in the lungs. First, we estibalish that ICGs can considerably impact host immunity and efficacy of immunotherapy. Secondly, we identify <i>CD160</i>, <i>HLA-DOA</i>, and <i>VTCN1</i> to significantly downregulate as tumors progress from early-stage to advanced-stage. In addition, the expression of <i>CD86</i>, <i>HLA-DPB1</i>, and <i>HAVCR2</i> are significantly positively correlated with pulmonary inflammation. Finally, <i>HLA-A</i>, <i>HLA-B</i>, and <i>HLA-E</i> levels positively correlate to immune- and inflammation-associated <i>Lachnoclostridium dominance</i>. Taken together, our study uncovers ICG signatures linked to tumor progression and sheds light on the complex network of microbiota-host immunity interactions within the lung microenvironment. This study lays the groundwork for future mechanistic studies and underscores the significance of microbiota-host immunity interactions for predicting and tracking the response to cancer treatment.</p>","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147593870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Physiological genomicsPub Date : 2026-04-01Epub Date: 2026-03-23DOI: 10.1152/physiolgenomics.00291.2025
Danielle E Levitt, Yasuki Sekiguchi
{"title":"Detecting metabolic stress signals to optimize intense military training: a focus on extracellular vesicle cargo as a promising strategy.","authors":"Danielle E Levitt, Yasuki Sekiguchi","doi":"10.1152/physiolgenomics.00291.2025","DOIUrl":"10.1152/physiolgenomics.00291.2025","url":null,"abstract":"","PeriodicalId":20129,"journal":{"name":"Physiological genomics","volume":" ","pages":"195-198"},"PeriodicalIF":2.5,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147499058","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}