Communications Biology最新文献

Towards a universal understanding of sex ratio in termites.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-10 DOI: 10.1038/s42003-025-07771-z

Simon Hellemans, Thomas Bourguignon, Yves Roisin

{"title":"Towards a universal understanding of sex ratio in termites.","authors":"Simon Hellemans, Thomas Bourguignon, Yves Roisin","doi":"10.1038/s42003-025-07771-z","DOIUrl":"https://doi.org/10.1038/s42003-025-07771-z","url":null,"abstract":"Termites are eusocial cockroaches whose altruist caste is constituted of males and females. While sex ratio theory predicts a balanced investment between sexes in diploid organisms, extreme deviations are observed in termites, both in altruists and alate reproductives. Here, we expand the theoretical framework for the prediction of alate population sex ratio by considering partitioned sexual and parthenogenetic reproduction, and female/male relatedness asymmetries arising from their sex-linked chromosome complexes. We consider the viewpoint of either the primary reproductives or the altruists while accounting for the effect of caste developmental systems on the sex ratio. We compile all data on alate sex ratios available to date (97 species), and found the direction of the sex ratio bias to be consistent within major taxonomic groups. We test our models, along with models of intrasexual competition, on an exploratory set of 13 species with available demographic data. Our analyses indicate that the factors explaining bias in alate sex ratio are variable and include sexual dimorphism, sex-asymmetric inbreeding, imperfect use of sexual and parthenogenetic reproduction, sex-linked genomic inheritance, intrasexual competition and caste developmental constraints. Our study provides an integrative framework for sex ratio and conflicts in termites, and closes in on a universal theory.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"404"},"PeriodicalIF":5.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CIRP contributes to multiple organ damage in acute pancreatitis by increasing endothelial permeability.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-10 DOI: 10.1038/s42003-025-07772-y

Wuming Liu, Derek H Wu, Tao Wang, Mengzhou Wang, Yujia Xu, Yifan Ren, Yi Lyu, Rongqian Wu

{"title":"CIRP contributes to multiple organ damage in acute pancreatitis by increasing endothelial permeability.","authors":"Wuming Liu, Derek H Wu, Tao Wang, Mengzhou Wang, Yujia Xu, Yifan Ren, Yi Lyu, Rongqian Wu","doi":"10.1038/s42003-025-07772-y","DOIUrl":"https://doi.org/10.1038/s42003-025-07772-y","url":null,"abstract":"Acute pancreatitis can lead to systemic inflammation and multiple organ damage. Increased endothelial permeability is a hallmark of systemic inflammation. Several studies have demonstrated that cold-inducible RNA-binding protein (CIRP) functions as a proinflammatory factor in various diseases. However, its role in endothelial barrier dysfunction during acute pancreatitis remains unknown. To study this, acute pancreatitis was induced by two hourly intraperitoneal injections of 4.0 g/kg L-arginine in wild-type (WT) or CIRP knockout mice. Our results showed that CIRP levels in the pancreas, small intestine, lung, and liver were upregulated at 72 h after the induction of acute pancreatitis in WT mice. CIRP deficiency significantly attenuated tissue injury, edema, and extravasation of Evans blue in the pancreas, small intestine, lung, and liver at 72 h after L-arginine injection. Administration of C23, a specific antagonist of CIRP, at 2 h after the last injection of L-arginine also produced similar protective effects as CIRP knockout in mice. In vitro studies showed that recombinant CIRP caused a significant reduction in transcellular electric resistance in HUVEC monolayers. Immunocytochemical analysis of endothelial cells exposed to CIRP revealed an increased formation of actin stress fibers. VE-cadherin and β-catenin staining showed intercellular gaps were formed in CIRP-stimulated cells. Western blot analysis showed that CIRP induced SRC phosphorylation at TYR416. Exposure to the SRC inhibitor PP2 reduced CIRP-induced endothelial barrier dysfunction in HUVEC monolayers. In conclusion, blocking CIRP mitigates acute pancreatitis-induced multiple organ damage by alleviating endothelial hyperpermeability. Targeting CIRP may be a potential therapeutic option for acute pancreatitis.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"403"},"PeriodicalIF":5.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596431","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Protein disulfide isomerase is essential for osteoblast differentiation in mice. 蛋白二硫异构酶对小鼠成骨细胞分化至关重要

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-10 DOI: 10.1038/s42003-025-07824-3

Yue Lu, Aizhen Yang, Zhenzhen Zhao, Yue Han, Depei Wu, Yi Wu

{"title":"Protein disulfide isomerase is essential for osteoblast differentiation in mice.","authors":"Yue Lu, Aizhen Yang, Zhenzhen Zhao, Yue Han, Depei Wu, Yi Wu","doi":"10.1038/s42003-025-07824-3","DOIUrl":"https://doi.org/10.1038/s42003-025-07824-3","url":null,"abstract":"Protein disulfide isomerase (PDI) is an oxidoreductase responsible for the formation, reduction and isomerization of disulfide bonds of nascent proteins in endoplasmic reticulum (ER). So far, the role of PDI in bone biology has never been characterized using genetically-modified animal models. In this study we generated osteoblast- specific PDI-deficient mice by crossing PDI-floxed (PDIfl/fl) mice with Osx-Cre mice. Compared with their littermate control PDIfl/fl mice, homozygous osteoblast-knockout mice (Osx-Cre/PDIfl/fl) were embryonically lethal, but heterozygous knockout mice (Osx-Cre/PDIfl/wt) displayed significantly pronounced growth retardation and reduced bone length. Besides, the decreases in bone density, osteoblast and osteoclast numbers, collagen fiber content and bone formation rate were observed in Osx-Cre/PDIfl/wt mice. Osteoblast precursors isolated from PDIfl/fl mice were infected with Cre recombinant adenovirus to produce PDI-deficient osteoblasts, followed by induction of differentiation. Osteoblasts deficient of PDI had decreased alkaline phosphatase activity, mineralizing capacity, and differentiation. Quantitative protein mass spectrometry analysis and immunoblotting showed that PDI deficiency markedly decreased the expression of the α-subunits of collagen prolyl 4-hydroxylase (C-P4H), including P4HA1, P4HA2 and P4HA3. These results demonstrate that PDI plays an essential role in osteoblast differentiation and bone formation and is required for the expression of the α-subunit of C-P4H in osteoblasts.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"402"},"PeriodicalIF":5.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596446","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Impact of immune cell metabolism on membranous nephropathy and prospective therapy.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-10 DOI: 10.1038/s42003-025-07816-3

Xuemei Duan, Xin Lv, Xiaocui Wang, Yunfei Zhang, Ying Hu, Haonan Li, Yongnian Zhou, Yukai Jing

{"title":"Impact of immune cell metabolism on membranous nephropathy and prospective therapy.","authors":"Xuemei Duan, Xin Lv, Xiaocui Wang, Yunfei Zhang, Ying Hu, Haonan Li, Yongnian Zhou, Yukai Jing","doi":"10.1038/s42003-025-07816-3","DOIUrl":"https://doi.org/10.1038/s42003-025-07816-3","url":null,"abstract":"Membranous nephropathy (MN) is a primary glomerular disease commonly causing adult nephrotic syndrome. Characterized by thickened glomerular capillary walls due to immune complex deposition, MN is a complex autoimmune disorder. Its pathogenesis involves immune deposit formation, complement activation, and a heightened risk of renal failure. Central to MN is immune system dysfunction, particularly the dysregulation of B and T cell responses. B cells contribute to renal injury through the production of autoantibodies, particularly IgG targeting the phospholipase A2 receptor (PLA2R) on podocytes, while T cells modulate immune responses that influence disease progression. Metabolic reprogramming alters lymphocyte survival, differentiation, proliferation, and function, potentially triggering autoimmune processes. Although the link between immune cell metabolism and MN remains underexplored, this review highlights recent advances in understanding immune metabolism and its role in MN. These insights may provide novel biomarkers and therapeutic strategies for MN treatment.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"405"},"PeriodicalIF":5.2,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143596437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Developmental air pollution exposure augments airway hyperreactivity, alters transcriptome, and DNA methylation in female adult progeny.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07835-0

Razia Zakarya, Yik Lung Chan, Baoming Wang, Andrew Thorpe, Dikaia Xenaki, Kin Fai Ho, Hai Guo, Hui Chen, Brian G Oliver, Christopher O'Neill

{"title":"Developmental air pollution exposure augments airway hyperreactivity, alters transcriptome, and DNA methylation in female adult progeny.","authors":"Razia Zakarya, Yik Lung Chan, Baoming Wang, Andrew Thorpe, Dikaia Xenaki, Kin Fai Ho, Hai Guo, Hui Chen, Brian G Oliver, Christopher O'Neill","doi":"10.1038/s42003-025-07835-0","DOIUrl":"10.1038/s42003-025-07835-0","url":null,"abstract":"Maternal exposure to particulate air pollution increases the incidence and severity of asthma in offspring, yet the mechanisms for this are unclear. Known susceptibility loci are a minor component of this effect. We interrogate a mouse allergic airway disease model to assess epigenetic associations between maternal air pollution exposure and asthma responses in offspring. Maternal air pollution exposure increased allergic airway disease severity in adult offspring associated with a suppressed transcriptomic response. Control progeny showed differential expression of 2842 genes across several important pathways, whilst air pollutant progeny showed an 80% reduction in differentially expressed genes and abrogation of many pathway associations. Whole genome CpG methylome analysis following allergen challenge detected differential methylation regions across the genome. Differentially methylated regions were markedly reduced in air pollutant offspring, and this was most evident in intronic regions and some transposable element classes. This study shows that asthma in adult offspring of PM2.5 exposed mothers had a markedly repressed transcriptomic response, a proportion of which was associated with identifiable changes in the lung's methylome. The results point to an epigenetic contribution to the severity of asthma in offspring of mothers exposed to particulate air pollution.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"400"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Melatonin affects trophoblast epithelial-to-mesenchymal transition and oxidative damage resistance by modulating GDF15 expression to promote embryo implantation.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07834-1

Guang Yang, Guidong Yao, Huihui Wang, Ran Jiang, Junnan Fang, Jingyi Hu, Yue Kong, Haixia Jin, Wenyan Song, Zhaoting Wu, Xianju Huang, Yingpu Sun

{"title":"Melatonin affects trophoblast epithelial-to-mesenchymal transition and oxidative damage resistance by modulating GDF15 expression to promote embryo implantation.","authors":"Guang Yang, Guidong Yao, Huihui Wang, Ran Jiang, Junnan Fang, Jingyi Hu, Yue Kong, Haixia Jin, Wenyan Song, Zhaoting Wu, Xianju Huang, Yingpu Sun","doi":"10.1038/s42003-025-07834-1","DOIUrl":"10.1038/s42003-025-07834-1","url":null,"abstract":"Melatonin is widely observed in the female reproductive system and regulates trophoblast cell functions, but its effects on embryo implantation and underlying mechanisms are not well understood. By constructing an in vitro embryo culture model, we found that melatonin enhances migration and implantation in human and mouse trophoblast cells. It also significantly promoted HTR-8/SVneo cell proliferation, inhibited apoptosis, enhanced migration, and mitigated oxidative damage. Further investigation revealed that melatonin promoted trophoblast cell migration and increased the in vitro implantation rate of HTR-8/SVneo spheroids by promotes epithelial-mesenchymal transition (EMT) via the growth differentiation factor 15 (GDF15)-mothers against decapentaplegic homolog 2/3 (SMAD2/3) pathway. Additionally, melatonin increased the levels of glutathione peroxidase 4 (GPX4) and glutathione (GSH) in HTR-8/SVneo cells by upregulating the expression of GDF15, inhibiting reactive oxygen species (ROS) accumulation, and increasing mitochondrial membrane potential, thus suppressing apoptosis during oxidative stress. In conclusion, melatonin promotes EMT in trophoblast cells via GDF15-SMAD2/3 pathway and partially induces the expression of GPX4 through GDF15 to enhance oxidative damage resistance in trophoblast cells. These findings highlight melatonin's regulatory role in embryo implantation and suggest new avenues for exploring its biological effects in reproduction and clinical applications.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"396"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890731/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585095","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Extravascular coagulation regulates haemostasis independently of activated platelet surfaces in an in vivo mouse model.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07838-x

Asuka Sakata, Kohei Tatsumi, Naoki Matsumoto, Nigel Mackman, Suguru Harada, Ryohei Kawasaki, Yukiko Okuyama-Nishida, Tetsuhiro Soeda, Keiji Nogami, Midori Shima

{"title":"Extravascular coagulation regulates haemostasis independently of activated platelet surfaces in an in vivo mouse model.","authors":"Asuka Sakata, Kohei Tatsumi, Naoki Matsumoto, Nigel Mackman, Suguru Harada, Ryohei Kawasaki, Yukiko Okuyama-Nishida, Tetsuhiro Soeda, Keiji Nogami, Midori Shima","doi":"10.1038/s42003-025-07838-x","DOIUrl":"https://doi.org/10.1038/s42003-025-07838-x","url":null,"abstract":"While the conventional understanding of haemostatic plug formation is that coagulation proceeds efficiently on the surface of activated platelets at the vascular injury site to form a robust haemostatic plug, this understanding does not explain the clinical reality that platelet dysfunction results in a mild bleeding phenotype, whereas coagulation disorders exhibit severe bleeding phenotypes, particularly in deep tissues. Here, we introduce an in vivo imaging method to observe internal bleeding and subsequent haemostatic plug formation in mice and report that haemostatic plug formation after internal bleeding, coagulation occurs primarily outside the blood vessel rather than on platelets. Experiments in mice with impaired platelet surface coagulation, depleted platelets, haemophilia A or reduced tissue factor expression suggest that this extravascular coagulation triggers and regulates haemostatic plug formation. Our discovery of the important role of extravascular coagulation in haemostasis may contribute to refining the treatment of haemostatic abnormalities and advancing antithrombotic therapy.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"390"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585069","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

FpnA, the Aspergillus fumigatus homolog of human ferroportin, mediates resistance to nickel, cobalt and gallium but does not function in iron homeostasis.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07799-1

Isidor Happacher, Simon Oberegger, Beate Abt, Annie Yap, Patricia Caballero, Mario Aguiar, Javeria Pervaiz, Giacomo Gariglio, Matthias Misslinger, Clemens Decristoforo, Hubertus Haas

{"title":"FpnA, the Aspergillus fumigatus homolog of human ferroportin, mediates resistance to nickel, cobalt and gallium but does not function in iron homeostasis.","authors":"Isidor Happacher, Simon Oberegger, Beate Abt, Annie Yap, Patricia Caballero, Mario Aguiar, Javeria Pervaiz, Giacomo Gariglio, Matthias Misslinger, Clemens Decristoforo, Hubertus Haas","doi":"10.1038/s42003-025-07799-1","DOIUrl":"10.1038/s42003-025-07799-1","url":null,"abstract":"Iron homeostasis is key to both the survival of virtually all organisms and the virulence of fungi including Aspergillus fumigatus, a human fungal pathogen causing life-threatening invasive infections. Unlike the extensively studied fungal species Saccharomyces cerevisiae and Schizosaccharomyces pombe, A. fumigatus encodes an uncharacterized homolog of vertebrate ferroportin (Fpn1), termed FpnA. Fpn1 is the only known vertebrate iron efflux transporter, while microbial organisms are thought to lack iron efflux systems. After correcting the exon-intron annotation, inactivation and conditional overexpression of the A. fumigatus FpnA-encoding gene (fpnA) indicated, that FpnA mediates resistance to nickel, cobalt and gallium but not to iron, aluminium, cadmium, copper or zinc. Functional N-terminal tagging with a fluorescent protein demonstrated localization of FpnA in the vacuolar membrane, suggesting that FpnA detoxifies substrate metals by vacuolar deposition. In line, overexpression of fpnA reduced the utilization of urea as a nitrogen source, most likely by depriving cytosolic urease of its essential cofactor nickel. Phylogenetic analysis illustrated conservation of FpnA in all fungal divisions and several other eukaryotic lineages, underlining its crucial role in metal homeostasis. The divergent localization and functionalization of ferroportin homologs in two phylogenetic sister groups, metazoa and fungi, is of particular evolutionary interest.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"399"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585074","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07742-4

Gege He, Pingping Liu, Xiaoyan Xuan, Min Zhang, Hongxia Zhang, Ka Yang, Yusheng Luan, Qian Yang, Jingyuan Yang, Qianru Li, Huaixin Zheng, Peng Wang

{"title":"Transcription factor ELF-1 protects against colitis by maintaining intestinal epithelium homeostasis.","authors":"Gege He, Pingping Liu, Xiaoyan Xuan, Min Zhang, Hongxia Zhang, Ka Yang, Yusheng Luan, Qian Yang, Jingyuan Yang, Qianru Li, Huaixin Zheng, Peng Wang","doi":"10.1038/s42003-025-07742-4","DOIUrl":"10.1038/s42003-025-07742-4","url":null,"abstract":"Inflammatory bowel disease (IBD) is a chronic, relapsing, and remitting disease characterized by chronic inflammation in the gastrointestinal tract. The exact etiology and pathogenesis of IBD remain elusive. Although ELF-1 has been known to be highly expressed in epithelial cells for past twenty years, little is known about its function in epithelial cells and epithelial-related IBD. Here, we demonstrated that ELF-1 deficiency in mouse lead to exacerbated DSS-induced colitis, marked by inflammation dominated by neutrophil infiltration and activation of IL-17 signaling pathways in various immune cells, including Th17, ILC3, γδT and NKT cells. Bone marrow transfer experiments confirmed ELF-1 deficiency in non-hematopoietic cells intrinsically worsened DSS-induced colitis. On one hand, ELF-1 deficiency enhanced the production of pro-inflammatory chemokines in colonic epithelial cells, leading to extensive infiltration of neutrophils and other immune cells into the colonic mucosal tissue. On the other hand, ELF-1 directly regulated the expression of the Rack1 gene in colonic epithelial tissue, which has been proved to play critical roles in maintaining intestinal homeostasis. Altogether, ELF-1 plays a protective role in colitis by maintaining intestinal epithelium homeostasis.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"395"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584202","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Transcriptional dynamics in type 2 diabetes progression is linked with circadian, thermogenic, and cellular stress in human adipose tissue.

IF 5.2 1区生物学

Communications Biology Pub Date : 2025-03-08 DOI: 10.1038/s42003-025-07709-5

Irais Rivera-Alvarez, Rosa Vázquez-Lizárraga, Lucía Mendoza-Viveros, Israim Sotelo-Rivera, Tannia L Viveros-Ruiz, Jesús Morales-Maza, Lorena Orozco, Marta C Romano, Lilia G Noriega, Armando R Tovar, Lorena Aguilar-Arnal, Ivette Cruz-Bautista, Carlos Aguilar-Salinas, Ricardo Orozco-Solis

{"title":"Transcriptional dynamics in type 2 diabetes progression is linked with circadian, thermogenic, and cellular stress in human adipose tissue.","authors":"Irais Rivera-Alvarez, Rosa Vázquez-Lizárraga, Lucía Mendoza-Viveros, Israim Sotelo-Rivera, Tannia L Viveros-Ruiz, Jesús Morales-Maza, Lorena Orozco, Marta C Romano, Lilia G Noriega, Armando R Tovar, Lorena Aguilar-Arnal, Ivette Cruz-Bautista, Carlos Aguilar-Salinas, Ricardo Orozco-Solis","doi":"10.1038/s42003-025-07709-5","DOIUrl":"10.1038/s42003-025-07709-5","url":null,"abstract":"The prevalence of type 2 diabetes (T2D) has increased significantly over the past three decades, with an estimated 30-40% of cases remaining undiagnosed. Brown and beige adipose tissues are known for their remarkable catabolic capacity, and their ability to diminish blood glucose plasma concentration. Beige adipose tissue can be differentiated from adipose-derived stem cells or through transdifferentiation from white adipocytes. However, the impact of T2D progression on beige adipocytes' functional capacity remains unclear. Transcriptomic profiling of subcutaneous adipose tissue biopsies from healthy normal-weight, obese, prediabetic obese, and obese subjects diagnosed with T2D, reveals a progressive alteration in cellular processes associated with catabolic metabolism, circadian rhythms, thermogenesis-related signaling pathways, cellular stress, and inflammation. MAX is a potential transcription factor that links inflammation with the circadian clock and thermogenesis during the progression of T2D. This study unveils an unrecognized transcriptional circuit that increasingly disrupts subcutaneous adipose tissue oxidative capacity during the progression of T2D. These findings could open new research venues for developing chrono-pharmaceutical strategies to treat and prevent T2D.","PeriodicalId":10552,"journal":{"name":"Communications Biology","volume":"8 1","pages":"398"},"PeriodicalIF":5.2,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11890630/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143584612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0