Hereditas最新文献

{"title":"Identification and validation of biomarkers associated with mitotic catastrophe in high-altitude hypoxia.","authors":"Wenwen Zhao, Defang Liu, Ting Luo, Yang Wu","doi":"10.1186/s41065-026-00692-9","DOIUrl":"https://doi.org/10.1186/s41065-026-00692-9","url":null,"abstract":"<p><strong>Background: </strong>High-altitude hypoxia (HAH) can cause adverse reactions, such as tinnitus and barotrauma, but the role of mitotic catastrophe (MC) in HAH remains unreported. This study investigated MC-associated biomarkers in HAH.</p><p><strong>Methods: </strong>HAH-related datasets and MC-related genes (MC-RGs) were retrieved from public databases. Differentially expressed genes (DEGs) between the HAH and control groups were screened, and overlapping genes between DEGs and MC-RGs were defined as candidates. Biomarkers were identified using three machine learning methods, receiver operating characteristic curve analysis, and expression validation. A nomogram was constructed for diagnostic assessment. Functional enrichment, immune infiltration, regulatory network, and drug prediction analyses were performed, with biomarker expression verified by reverse transcription quantitative polymerase chain reaction (RT-qPCR).</p><p><strong>Results: </strong>DIAPH1 and MDM4 were confirmed as MC-associated biomarkers in HAH, and the nomogram displayed excellent diagnostic ability (area under the curve = 0.929). These biomarkers were coenriched in pathways such as oxidative phosphorylation. DIAPH1 was positively correlated with the infiltration of resting NK cells, whereas MDM4 was negatively correlated with that of M2 macrophages. A transcription factor-mRNA-miRNA network was established, with USF2 and GATA2 jointly targeting both biomarkers. Drugs such as rescinnamine targeted MDM4. RT-qPCR verified that USF2 and GATA2 were significantly downregulated in HAH (both P < 0.01), consistent with the bioinformatics results.</p><p><strong>Conclusions: </strong>DIAPH1 and MDM4 are valid MC-associated biomarkers for HAH. This study provides novel insights into HAH prevention and treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.5,"publicationDate":"2026-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147987140","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":"Identification and validation of lactylation-related genes signature and immune infiltration landscape of rheumatoid arthritis based on machine learning.","authors":"Xiaoli Hu, Qian Xiao, Lizhou Wang, Yuan Xu, Qiaoqiao Gou, Jing Wen, Shi Zhou","doi":"10.1186/s41065-025-00579-1","DOIUrl":"10.1186/s41065-025-00579-1","url":null,"abstract":"<p><strong>Background: </strong>The pathogenic mechanisms underlying rheumatoid arthritis (RA) remain elusive. Lactylation, a novel post-translational modification, may regulate immune and metabolic reprogramming, underscoring the imperative to delineate lactylation-related genes (LRGs) driving RA progression.</p><p><strong>Methods: </strong>LRG expression profiles from RA patients and healthy controls were analyzed from GEO datasets. Immune infiltration and LRG-immune correlations were assessed. A machine-learning framework identified a hub LRG signature, whose metabolic and therapeutic relevance was evaluated via functional enrichment and druggability analyses. qRT-PCR validated hub gene expression in RA MH7A cells model.</p><p><strong>Results: </strong>Transcriptomic profiling identified 36 differentially expressed LRGs regulating cytokine networks and immune signaling in RA. Disease stratification revealed two molecular subtypes, with Subtype B demonstrating p53 signaling and innate immunity pathway activation via gene set variation analysis (GSVA). Weighted correlation network analysis (WGCNA) identified subtype B-associated modules (504 genes). A machine learning-derived 7-LRG signature (Sdc1, Pfkfb1, Fut8, Adh1b, Kif23, Adh1c, Pkc1) differentiated RA from controls (AUC 0.92). Single-cell resolution analysis localized Sdc1 to plasma cell clusters, correlating with memory B cell expansion and macrophage polarization. Hub LRGs were enriched in glucose metabolism pathways in RA, and Sdc1, Adh1b, and Adh1c were druggable, suggesting potential therapeutic targets. qRT-PCR validation confirmed significant LRG upregulation in RA cellular models.</p><p><strong>Conclusion: </strong>Our findings establish lactylation as a key modulator of immune dysregulation in RA pathogenesis. Seven LRG biomarkers were identified and validated, exhibiting dual potential as prognostic indicators and therapeutic targets through lactylation-driven pathway modulation for RA.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343758/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147941147","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}

{"title":"LncRNA HOXA11-AS promotes idiopathic pulmonary fibrosis progression via sponging miR-148a-3p and regulating SMAD2.","authors":"Lidong Wang, Xing Ding, Ran Tang, Heping Jiang","doi":"10.1186/s41065-026-00684-9","DOIUrl":"10.1186/s41065-026-00684-9","url":null,"abstract":"<p><strong>Background: </strong>Idiopathic Pulmonary Fibrosis (IPF) is characterized primarily by progressive lung tissue scarring. This study aimed to explore the molecular mechanism of the HOXA11-AS/miR-148a-3p/SMAD2 axis in IPF.</p><p><strong>Methods: </strong>Sixty IPF patients and 70 healthy controls were recruited. mRNA expression was measured by RT-qPCR. An IPF model was established in A549 cells and MRC-5 cells using transforming growth factor-beta 1 (TGF-β1) induction. Cell proliferation, apoptosis, oxidative stress levels, and fibrosis markers were assessed using the cell counting kit-8 (CCK-8), flow cytometry, and enzyme-linked immunosorbent assay (ELISA), respectively. A dual-luciferase reporter assay was conducted to confirm the regulatory interaction.</p><p><strong>Results: </strong>In IPF patients, HOXA11-AS expression was significantly upregulated. Its expression was negatively correlated with lung function parameters as well as with the 6-minute walk test (6MWT) distance. Conversely, it was positively associated with fibrosis-related serum markers, such as hyaluronic acid (HA) and laminin (LN). These findings suggested that HOXA11-AS may serve as a promising diagnostic biomarker for IPF. Moreover, HOXA11-AS promoted the proliferation, suppressed apoptosis, enhanced oxidative stress by reducing superoxide dismutase (SOD) activity and increasing malondialdehyde (MDA) levels, and upregulated the key fibrosis markers expression, including alpha-smooth muscle actin (α-SMA), Collagen I, and Fibronectin. HOXA11-AS directly binds to miR-148a-3p, which in turn targets and regulates SMAD2. Notably, inhibition of miR-148a-3p reversed the suppressive effects of HOXA11-AS knockdown on TGF-β1-induced proliferation, oxidative stress, and fibrotic phenotypes in A549 cells, while restoring SMAD2 expression. Consistent results were observed in MRC-5 fibroblasts: HOXA11-AS knockdown significantly attenuated TGF-β1-induced proliferation, promoted apoptosis, and decreased the expression of α-SMA, Collagen I, and Fibronectin. These effects were partially reversed by miR-148a-3p inhibition, confirming the functional role of the HOXA11-AS/miR-148a-3p/SMAD2 axis in lung fibroblasts.</p><p><strong>Conclusions: </strong>HOXA11-AS promoted the IPF progression by upregulating SMAD2 expression through the sponging of miR-148a-3p.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343633/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147941246","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}

{"title":"MiR-642a-3p increases the risk of postmenopausal osteoporosis and fractures by targeting INO80.","authors":"Jingyu Zhang, Han Xiao","doi":"10.1186/s41065-026-00689-4","DOIUrl":"10.1186/s41065-026-00689-4","url":null,"abstract":"<p><strong>Background: </strong>Postmenopausal osteoporosis (PMO), a metabolic bone disorder from estrogen deficiency, disrupts the balance between bone resorption and formation. Its severe consequence, osteoporotic fractures (OPF), significantly increases disability and mortality, severely impacting patients' quality of life. Elevated miR-642a-3p has been identified in both PMO and bone loss. This research aims to further explore the role of miR-642a-3p in predicting PMO development and OPF risk, along with its underlying mechanisms.</p><p><strong>Results: </strong>The research enrolled 127 PMO patients and 91 healthy volunteers (HV). And further subdivided the PMO group into osteoporotic fractures (n = 62) subgroup and without fractures (OPNF, n = 65) subgroup. The results indicate that miR-642a-3p was significantly upregulated in both the PMO and OPF groups. MiR-642a-3p demonstrated good predictive performance for PMO occurrence and OPF risk. High miR-642a-3p expression was identified as an independent risk factor for progression from PMO to OPF. Downregulation of miR-642a-3p not only stimulated osteoblast proliferation but also mitigated associated inflammation and oxidative stress. Furthermore, INO80 is targeted and regulated by miR-642a-3p.</p><p><strong>Conclusion: </strong>MiR-642a-3p may have potential as a biomarker for future clinical prediction of PMO and OPF. Inhibition of miR-642a-3p promotes osteoblast proliferation, associated inflammation, and oxidative stress by upregulation of INO80 expression.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13343866/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147928697","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}

{"title":"E2F2 and TFDP1 as novel systemic lupus erythematosus (SLE) diagnostic markers and therapeutic targets based on machine learning and experimental study.","authors":"Qingbo Pan, Xuliang Yu, Jin Zhu, Xiaojin Zheng","doi":"10.1186/s41065-026-00687-6","DOIUrl":"10.1186/s41065-026-00687-6","url":null,"abstract":"<p><strong>Background: </strong>Systemic lupus erythematosus (SLE) is a chronic autoimmune disease influenced by multiple genetic and environmental factors.. This study used bioinformatics to identify new diagnostic biomarkers and explore the pathogenesis of SLE.</p><p><strong>Method: </strong>Three array datasets of peripheral blood mononuclear cells (PBMCs) from SLE patients and control subjects were obtained from GEO, including GSE82221 and GSE11909 (merged for feature discovery) and GSE154851 (independent validation/machine learning training dataset). RRA analysis was used to identify statistically changed DEGs. GO and KEGG analyses explored biological mechanisms. Consistent clustering and machine learning models were employed to identify diagnostic biomarkers, further assessed using ROC and DCA analysis. The proportions of 22 immune cells in SLE patients were calculated via CIBERSORT algorithm, and correlations between biomarkers and immune cells were explored. Data from 76 clinical blood samples were collected, including ALT, AST, CR, BUN, CRP, PLT, WBC, lymphocyte (%), and neutrophil (%). RT-qPCR was used to validate the expression of diagnostic biomarkers.</p><p><strong>Results: </strong>A total of 62 DEGs were identified, mainly involved in the cell cycle and TGF-beta signaling pathway. Six candidate diagnostic biomarkers for SLE were found: E2F2, KIAA0319L, TRIM58, MMP8, FKBP5, and TFDP1. E2F2 and TFDP1 showed AUC values > 0.7 in training and validation datasets. CIBERSORT analysis revealed disturbed immune cell types in SLE patients, with plasma cells most relevant to E2F2 and TFDP1 expression. Expression of E2F2 and TFDP1 was upregulated in patient samples. The diagnostic models, including E2F2 and TFDP1, performed better than those without these biomarkers.</p><p><strong>Conclusion: </strong>Our study identifies E2F2 and TFDP1 as potential diagnostic biomarkers for SLE patients and uncovers their most relevant immune cells.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13330141/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868109","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}

{"title":"Expression of long non-coding RNA NNT-AS1 in children with severe pneumonia and its effect on lipopolysaccharide-induced human embryonic lung fibroblast injury.","authors":"Fanghua Jian, Jun Fu, Dan Li, Weiqiang Bao","doi":"10.1186/s41065-026-00683-w","DOIUrl":"10.1186/s41065-026-00683-w","url":null,"abstract":"<p><strong>Background: </strong>Severe pneumonia (SP) threatens the quality of life and well-being of children. This study aims to explore the serum NNT-AS1 expression in SP children and its impact on lipopolysaccharide (LPS)-induced injury in human embryonic lung fibroblasts.</p><p><strong>Methods: </strong>The study included 69 SP children, 62 mild pneumonia (MP) children and 75 healthy controls. A pneumonia cell model was constructed with LPS-induced MRC-5 cells. Loss-of-function experiments were performed using si-NNT-AS1 and miR-23a-3p inhibitor. The NNT-AS1 and miR-23a-3p expression was detected by real-time quantitative polymerase chain reaction. The diagnostic effect and prognostic value of NNT-AS1 were evaluated by receiver operating characteristics curves and Kaplan-Meier method. Cell viability and apoptosis were determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay and flow cytometry. Inflammatory factors were measured by enzyme-linked immunosorbent assay. The interaction between NNT-AS1 and miR-23a-3p was verified by luciferase reporter gene and RNA immunoprecipitation assays. Pearson correlation coefficient was used to analyze the correlation.</p><p><strong>Results: </strong>NNT-AS1 was upregulated in SP children and showed good diagnostic efficacy (area under the curve (AUC) = 0.815). High NNT‑AS1 expression predicted a poorer survival. Silencing of NNT-AS1 increased cell viability, decreased apoptosis, and alleviated inflammatory responses. MiR-23a-3p was a target of NNT-AS1. Inhibition of miR-23a-3p partially reversed the protective effects of NNT-AS1 silencing on LPS-induced MRC-5 cell injury.</p><p><strong>Conclusions: </strong>Serum NNT-AS1 is upregulated in SP patients, and its expression is correlated with clinical prognosis. NNT-AS1 participates in LPS-induced cellular damage by regulating miR-23a-3p. These findings provide a new theoretical basis for understanding the pathogenesis of SP.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13326398/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147863831","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}

{"title":"Diagnostic value of LncRNA JPX in osteoporotic fracture (OPF) and its role in inhibiting osteogenic differentiation by targeting miR-219a-5p.","authors":"Junli Li, Yiwei Li, Ningning Zhang, Zhijian Cheng","doi":"10.1186/s41065-026-00685-8","DOIUrl":"10.1186/s41065-026-00685-8","url":null,"abstract":"<p><strong>Background: </strong>This study was designed to investigate the diagnostic potential of the long non-coding RNA JPX in osteoporotic fractures (OPF) and to explore its functional role in the regulation of fracture healing.</p><p><strong>Methods: </strong>A total of 244 patients with osteoporosis were enrolled, including 110 with osteoporosis (OP) and 134 with OPF. Expression levels of JPX, miR-219a-5p, and osteogenic markers (OPG, ALP, Collagen I, OCN) were detected by RT-qPCR. ROC analysis was employed to assess the clinical value of JPX. In human bone marrow mesenchymal stem cells (hBMSCs), gain- and loss-of-function experiments were performed to modulate JPX and miR-219a-5p expression. Cell proliferation was evaluated by CCK-8 assay. Flow cytometry assessed apoptosis. Dual luciferase reporter assays and RIP experiments validated the targeting relationship between JPX and miR-219a-5p.</p><p><strong>Results: </strong>JPX was upregulated in the OPF group, with good diagnostic performance (AUC = 0.897; specificity = 76.87%; sensitivity = 84.55%), and JPX was identified an independent predictive factor. DFH and NFH could also be distinguished. JPX upregulation inhibited proliferation, promoted apoptosis, and suppressed osteogenic markers and ALP activity. JPX largely resides in the cytoplasm and directly binds miR-219a-5p, forming a ceRNA axis; upregulation of miR-219a-5p could reverse these effects.</p><p><strong>Conclusion: </strong>JPX is associated with fracture risk and delayed healing, potentially influencing osteogenesis by sponge-like regulation of miR-219a-5p.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13289444/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814219","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}

{"title":"STEAP2-associated modulation of PI3K/AKT/mTOR signaling contributes to ginkgetin-induced apoptosis in bladder cancer cells.","authors":"Pengze Wu, Lin Chen, Jin Yang, Zhengkang Liang, Xiaofeng Yin, Shaowen Zhou, Zhilin Deng, Yafei Yang","doi":"10.1186/s41065-026-00686-7","DOIUrl":"10.1186/s41065-026-00686-7","url":null,"abstract":"<p><strong>Background: </strong>Bladder cancer remains a major urologic malignancy with substantial recurrence and progression risk, underscoring the need for mechanism-informed therapeutic candidates. Ginkgetin, a biflavonoid derived from Ginkgo biloba leaves, has shown antitumor potential in several cancer settings, yet its key signaling axis and actionable molecular node in bladder cancer have not been systematically defined.</p><p><strong>Methods: </strong>We evaluated ginkgetin across multiple bladder cancer cell lines (5637, T24, HT-1376, J82) and normal urothelial cells (SV-HUC-1) using viability assays and IC₅₀ estimation. Antitumor phenotypes were assessed by colony formation, wound-healing migration assays, EMT marker profiling, and Annexin V/PI flow cytometry. Network pharmacology and RNA-seq were integrated to prioritize enriched pathways, followed by western blot validation of PI3K/AKT/mTOR phosphorylation. An insulin reactivation (\"rescue\") strategy was used to functionally test pathway dependence. Transcriptome-derived candidates were further examined by RT-qPCR and STEAP2 overexpression to probe node-level involvement. In addition, molecular docking and 100-ns molecular dynamics simulations were performed to characterize ligand-target binding stability.</p><p><strong>Results: </strong>Ginkgetin suppressed bladder cancer cell viability in a time- and dose-dependent manner at low micromolar concentrations, while normal urothelial cells required markedly higher exposures. Functionally, ginkgetin reduced clonogenic survival, inhibited migration, and shifted EMT features toward an epithelial phenotype. Apoptosis increased in parallel, accompanied by a pro-apoptotic protein signature. Multi-omics and network analyses converged on PI3K-Akt signaling, and experimental validation showed that ginkgetin primarily dampened pathway output by reducing PI3K/AKT/mTOR phosphorylation rather than total protein abundance. Insulin-mediated reactivation partially reversed phosphorylation suppression and attenuated apoptosis-related shifts, supporting a functional link between axis inactivation and apoptotic tendency. STEAP2 was consistently downregulated after treatment, and STEAP2 overexpression partially counteracted apoptosis-associated changes.</p><p><strong>Conclusion: </strong>These findings support a coherent \"phenotype-pathway-node\" model in which ginkgetin inhibits malignant phenotypes and promotes apoptosis in bladder cancer cells, associated with reduced PI3K/AKT/mTOR activity and STEAP2 downregulation. The PI3K/AKT/mTOR axis and STEAP2 emerge as testable mechanistic entry points for further translational validation.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13288564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147814228","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}

{"title":"Identification and validation of biomarkers related to lysine β-hydroxybutyrylation in chronic obstructive pulmonary disease based on transcriptomics data.","authors":"Jing Lei, Jing Zhang, Linfei Yang, Yubao Chen","doi":"10.1186/s41065-026-00682-x","DOIUrl":"10.1186/s41065-026-00682-x","url":null,"abstract":"<p><p>BACKGROUND: Chronic obstructive pulmonary disease (COPD) involves progressive lung inflammation and tissue destruction. Lysine β-hydroxybutyrylation (Kbhb) is linked to COPD. This study aimed to identify Kbhb-related biomarkers for COPD to aid therapeutic development. METHODS: COPD data and Kbhb-related genes (Kbhb-RGs) were obtained from public databases and literature. Candidate genes were identified by overlapping differentially expressed genes (DEGs) with Kbhb-RGs. Biomarkers were selected using machine learning. Diagnostic efficacy was evaluated via a nomogram. Functional enrichment, immune infiltration, drug prediction, and molecular docking analyses were performed. Biomarker expression was validated by reverse transcription quantitative polymerase chain reaction (RT-qPCR). RESULTS: A total of 12 candidate genes were detected at the intersection of 765 DEGs and 1,493 Kbhb-RGs. Subsequently, POLD2 and OTUD7B were identified as biomarkers, and the expression of these 2 genes was found to be downregulated in COPD samples. The nomogram developed utilizing these biomarkers demonstrated a satisfactory capacity for differentiating among various sample types. Biomarkers were significantly enriched in transcriptional regulation and translation processes. Regulatory T cells displayed a significant positive linkage with OTUD7B (correlation (r) > 0.3, P < 0.05). Eosinophils were considerably negatively relevant to POLD2 and OTUD7B (r < -0.3, P < 0.05). Molecular docking studies demonstrated a strong binding affinity between biomarkers and estradiol. Compared with the control group, the expression levels of POLD2 and OTUD7B were significantly lower in the COPD group. CONCLUSIONS: This study identified POLD2 and OTUD7B as biomarkers for COPD, offering valuable insights that could support the development of targeted therapies. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13245097/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769857","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}

{"title":"miR-1229-3p promotes epithelial-mesenchymal transition and metastasis of cervical cancer cells by targeting FBXL5.","authors":"Donglian Lan, Xiaojing Sun, Lei Yao, Bo Cao","doi":"10.1186/s41065-026-00679-6","DOIUrl":"10.1186/s41065-026-00679-6","url":null,"abstract":"<p><p>OBJECTIVE: This study aimed to explore the biological function of miR-1229-3p in the occurrence and development of cervical cancer (CC). METHODS: The expression levels of miR-1229-3p and FBXL5 in CC tissues and cell lines were detected by RT-qPCR. Cell proliferation ability was evaluated by MTT. Cell migration and invasion abilities were detected by Transwell. The expression of EMT-related markers were detected by RT-qPCR. The targeting relationship between miR-1229-3p and FBXL5 was verified by dual luciferase reporter assay. RESULTS: The expression of miR-1229-3p was significantly upregulated in CC tissues and CC cell lines. High expression of miR-1229-3p was associated with poor differentiation and lymph node metastasis. Overexpression of miR-1229-3p could promote the proliferation, migration, invasion of CC cells, and induce the EMT process. Dual luciferase reporter assays confirmed that FBXL5 was the direct target gene of miR-1229-3p, and their expressions showed a significant negative correlation in CC tissues. Overexpression of FBXL5 could reverse the carcinogenic effects caused by miR-1229-3p. CONCLUSION: miR-1229-3p directly inhibits the expression of FBXL5, thereby activating the EMT process, and ultimately promoting the proliferation, migration, and invasion of CC cells. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13237886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769948","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}