Hereditas最新文献

{"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}

{"title":"Identification of biomarkers related to γ-aminobutyric acid-associated genes in membranous nephropathy based on transcriptome data and clinical experiments.","authors":"Jie Luo, Min Chen, Jing Li, Yue Qi, Tingyu Chen, Huibin Nie","doi":"10.1186/s41065-026-00681-y","DOIUrl":"10.1186/s41065-026-00681-y","url":null,"abstract":"<p><p>BACKGROUND: Membranous nephropathy (MN) is a leading cause of nephrotic syndrome in adults, being driven by incompletely understood autoimmune mechanisms. Emerging evidence suggests that γ-aminobutyric acid (GABA), traditionally considered a neurotransmitter, also functions as a critical immunomodulator in peripheral tissues. Dysregulation of GABAergic signaling has been linked to altered immune cell trafficking and metabolic stress in renal pathologies. However, its specific role and signature genes in MN pathogenesis have not been systematically characterized. This study aimed to identify novel GABA-associated biomarkers for MN and elucidate their potential mechanistic roles. RESULTS: By integrating differential expression analysis, weighted gene coexpression network analysis, and machine learning algorithms on public transcriptomic datasets, we identified three robust GABA-associated candidate biomarkers: AP2S1, STXBP1, and GNGT2. These genes were consistently upregulated in patients with MN across both the training and validation cohorts. Functional enrichment analysis revealed their significant involvement in vesicle trafficking, cytochrome P450 metabolism, and cell adhesion pathways. Immune infiltration analysis demonstrated that these biomarkers had strong positive correlations with central memory CD4 + T cells and myeloid-derived suppressor cells. Furthermore, molecular docking simulations indicated high binding affinities between these targets and potential therapeutic compounds, including valproic acid and genistein. Crucially, reverse transcription quantitative polymerase chain reaction validation in an independent clinical cohort (n = 10) confirmed significantly elevated expression of AP2S1, STXBP1, and GNGT2 in the peripheral blood of patients with MN versus healthy controls (P < 0.05). CONCLUSION: This study established a distinct GABAergic signature in MN, highlighting AP2S1, STXBP1, and GNGT2 as promising noninvasive diagnostic biomarkers. Our findings suggested that GABA-related vesicle trafficking and metabolic pathways contribute to the autoimmune microenvironment in MN. These genes offer new avenues for early diagnosis and represent potential therapeutic targets for precision medicine strategies in managing MN. </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/PMC13237888/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769920","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":"A comprehensive analysis of the Cullin family reveals that CUL5 and CUL7 promote colorectal cancer progression and serve as prognostic markers.","authors":"Noura Al-Dayan","doi":"10.1186/s41065-026-00677-8","DOIUrl":"10.1186/s41065-026-00677-8","url":null,"abstract":"<p><p>Colorectal cancer (CRC) remains a major cause of cancer-related mortality worldwide. Although Cullin family genes (CUL1, CUL2, CUL3, CUL4A, CUL4B, CUL5, CUL7, and CUL9) have been implicated in tumorigenesis, their roles in CRC are not fully defined. This study integrated in silico analysis with in vitro validation to characterize the expression and functional relevance of these genes in CRC. Transcriptomic profiling of TCGA datasets revealed significant up-regulation of CUL1, CUL2, CUL4A, CUL4B, CUL5, CUL7, and CUL9 in tumor tissues, with higher expression correlating with advanced stage and poorer survival, particularly for CUL5 and CUL7. Immunohistochemistry confirmed elevated protein levels, while genomic analysis showed that CUL9, CUL1, and CUL7 exhibited the highest mutation frequencies, though without significant survival impact. Single-cell and subtype analyses demonstrated distinct Cullin gene expression patterns across tumor-associated cell populations and immune or molecular subtypes. Functional enrichment indicated involvement in ubiquitin-mediated proteolysis and cancer-related pathways. Experimental knockdown of CUL5 and CUL7 in CRC cell lines significantly reduced proliferation and colony formation. ChIP-qPCR demonstrated increased H3K27ac enrichment at the CUL5 and CUL7 promoters in CRC cells, indicating epigenetic activation. Cycloheximide (CHX) chase assays further showed that silencing CUL5 or CUL7 accelerated the degradation of CREB1 and Cyclin D1, suggesting a role in substrate stabilization. Overall, our findings highlight the widespread up-regulation and functional significance of Cullin genes in CRC, with CUL5 and CUL7 emerging as key contributors to tumor progression and potential biomarkers or therapeutic targets.</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/PMC13238039/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769807","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":"Tussilagone mitigates sepsis-induced acute lung injury in mice by suppressing RIPK1 expression.","authors":"Jie Gu, Yachen Cai, Jiangwen Yin, Mengjie Zhang, Jun Chen, Hongjun Miao","doi":"10.1186/s41065-026-00678-7","DOIUrl":"10.1186/s41065-026-00678-7","url":null,"abstract":"<p><p>OBJECTIVE: Sepsis is a severe condition characterized by life-threatening organ dysfunction resulting from an excessive host response to infection. Among the affected organs, the lungs are particularly susceptible during the progression of sepsis. Tussilagone (TS), a sesquiterpenoid compound derived from the flowers of Tussilago farfara, has been explored for its potential therapeutic effects on sepsis-induced lung injury. This study used both in vitro and in vivo experimental approaches, complemented by network pharmacology analyses, to verify the mechanisms and molecular targets underlying the effects of TS. METHODS: TS was administered to mice with sepsis-induced lung injury and to lung epithelial cells stimulated with lipopolysaccharide (LPS) to assess its therapeutic potential. Inflammatory factor levels in mouse serum, lung tissue, and cells were assessed. Western blot analysis was used to determine the expression of NF-κB p65 and MyD88 in lung tissues. Potential molecular TS targets were identified, with receptor-interacting serine/threonine-protein kinase 1 (RIPK1) selected for further investigation using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform. Additionally, the study explored if TS exerts its protective effects against lung injury in septic mice through targeted regulation of RIPK1. RESULTS: TS inhibited the NF-κB p65 and MyD88 signaling pathways, reducing the release of inflammatory factors and a mitigation of lung injury severity in LPS-induced MLE12 cells and CLP-induced septic mice. Overexpression of RIPK1 protein resulted in elevated expression levels of NF-κB p65 and MyD88, whereas treatment with TS significantly reduced these levels. Similarly, the use of a RIPK1 protein inhibitor to suppress RIPK1 expression also decreased the expression of NF-κB p65 and MyD88, further supporting the role of RIPK1 in the mechanism of TS-mediated lung protection. CONCLUSION: TS demonstrates a protective effect against sepsis-induced acute lung injury (ALI) by inhibiting the expression of RIPK1. These findings indicate that TS can potentially be a therapeutic agent for the treatment of ALI. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13231789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147769906","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":"Hub genes of neutrophil extracellular traps in abdominal aortic aneurysm: a bioinformatics analysis.","authors":"Jinxin Liu, Bixuan Yue, Zhiying Shen, Bo Yang, Yuxuan Ou, Xiaowu Wang","doi":"10.1186/s41065-026-00663-0","DOIUrl":"10.1186/s41065-026-00663-0","url":null,"abstract":"<p><p>PURPOSE: This study aimed to identify the key genes involved in the development of AAA by various bioinformatics methods and explore their potential mechanisms. METHODS: Feature genes were screened by machine learning and other methods, and ROC curves were used to verify the model performance in the internal and external validation sets. Cluster analysis and immune infiltration analysis were then performed, and two key genes were finally determined and experimentally verified. GSEA, GO and KEGG analyses were performed. RESULTS: DEGs were identified by the “limma” package. DENETs were obtained by intersecting DEGs with NETs. GSEA, GO and KEGG analyses revealed that these genes were enriched in pathways such as cell response to lipopolysaccharide and chemokine signaling. Cluster analysis was performed to compare the expression differences of 25 DENETs between clusters, and immune infiltration analysis revealed immune dysregulation in AAA. Then, IL6 and PADI4 were finally identified as DENETs, and further GSEA analysis revealed that they were related to inflammation and immune response. In the wet experiment, IL6 and PADI4 finally showed expression trends consistent with the results of bioinformatics analysis. CONCLUSIONS: Our study identified IL6 and PADI4 as hub genes. They play an important role in promoting the development of AAA through inflammation, providing potential molecular targets for further treatment and intervention of AAA in the future. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-04-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13227812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147728811","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}