Hereditas最新文献

{"title":"14-3-3β knockdown inhibits migration and colony formation of esophageal squamous cell carcinoma cells and is associated with weakened p-AKT signaling.","authors":"Qing-Hua Hu, Man-Qin Zhu, Kuai Chen, Jin-Shi Huang, Qiang Tao, Zhi-Bin Guo","doi":"10.1186/s41065-026-00651-4","DOIUrl":"10.1186/s41065-026-00651-4","url":null,"abstract":"<p><p>OBJECTIVES: This study aims to explore the functions and mechanisms underlying the involvement of 14-3-3β in esophageal squamous cell carcinoma (ESCC). METHODS: Western blot and quantitative real-time PCR (RT-PCR) were utilized to evaluate the levels of 14-3-3β in SHEE, TE-1, and KYSE-150 cells. Following infection with YWHAB-RNAi lentivirus and puromycin screening, the reduction of 14-3-3β expression in KYSE-150 cells was confirmed via western blot and RT-PCR. Subsequently, wound healing, CCK8, and colony-formation assays were performed to assess cell migration and proliferation in KYSE-150 cells with stable low levels of 14-3-3β. Furthermore, western blot analysis was conducted to examine the expression of relevant proteins, elucidating the potential molecular mechanisms underlying 14-3-3β involvement in ESCC progression and metastasis. RESULTS: The expression of 14-3-3β was significantly elevated in KYSE-150 cells compared to SHEE cells. Upon infection in KYSE-150 cells, the expression of 14-3-3β was diminished, resulting in suppressed cell migration and colony formation, although no significant changes were observed in the CCK8 assays. Furthermore, in KYSE-150 cells exhibiting reduced 14-3-3β expression, the activity of phosphorylated AKT (p-AKT) was significantly decreased, while no notable difference was detected in AKT protein levels. Additionally, there were no significant alterations observed in apoptosis-related proteins, including BCL2, BAX, Caspase3, and activated Caspase9. CONCLUSIONS: In KYSE-150 cells infected with YWHAB-RNAi lentivirus, the downregulation of 14-3-3β expression resulted in significant reductions in both cell migration and proliferation. Furthermore, the findings demonstrated that 14-3-3β may regulate the biological activities of ESCC cells via modulation of the PI3K/AKT signaling pathway. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12998086/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146165001","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":"Clinical value of miR-551b-5p in children with primary nephrotic syndrome and its regulatory role in disease progression.","authors":"Yuehong Yang, Lijun Zhao, Fang Wu, Caihong Xue, Xiaoyun Qu","doi":"10.1186/s41065-026-00644-3","DOIUrl":"10.1186/s41065-026-00644-3","url":null,"abstract":"<p><p>BACKGROUND: Primary nephrotic syndrome (PNS) is a common glomerular disorder in children. Despite significant advances in glucocorticoid therapy, considerable challenges remain in the early diagnosis and prognostic management of PNS. Elevated miR-551b-5p expression has been detected in the PNS. This study aims to further explore the role of miR-551b-5p in the onset and progression of PNS and its potential mechanisms. METHODS: A total of 107 patients with primary nephrotic syndrome (PNS) and 99 healthy volunteers (HV) were included in this study. And the PNS group was further divided into subgroups with favorable (n = 76) and poor (n = 31) prognosis. The expression of miR-551b-5p in the PNS and the poor prognosis group was quantified using qRT-PCR. The predictive capability of miR-551b-5p for the occurrence and poor prognosis of PNS was evaluated. The effects of miR-551b-5p knockdown on podocyte growth and inflammatory injury were examined. The interaction between miR-551b-5p and CD2AP was verified via database and luciferase assay. RESULTS: miR-551b-5p is obviously elevated in PNS and the poor prognosis group. miR-551b-5p exhibits strong diagnostic capability for both the onset and poor prognosis of pediatric PNS. High miR-551b-5p expression is an independent risk factor for poor prognosis in pediatric PNS patients. miR-551b-5p downregulation potently promotes podocyte proliferation and reduces apoptosis, and improves intracellular inflammatory responses and oxidative stress levels. Furthermore, CD2AP is a direct target of miR-551b-5p, and this regulatory axis synergistically contributes to the pathogenesis and progression of PNS. CONCLUSION: miR-551b-5p is a potential biomarker for predicting the occurrence and poor prognosis of PNS. miR-551b-5p promotes the onset and progression of PNS by targeting CD2AP. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12983489/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146142358","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-4652-3p suppresses glutamine metabolism induced by the inflammatory microenvironment in non-small cell lung cancer by regulating MYC/SLC1A5.","authors":"Yihua Que, Yan Song, Deng Huang, Xianzhen Wu, Yang Pan","doi":"10.1186/s41065-026-00649-y","DOIUrl":"10.1186/s41065-026-00649-y","url":null,"abstract":"<p><p>BACKGROUND: MicroRNAs (miRNAs) play a crucial role in tumorigenesis and malignant transformation. Studies indicate that miR-4652-3p is aberrantly expressed in various cancer types. However, its impact and underlying mechanisms in non-small cell lung cancer (NSCLC) have not been investigated. METHODS: A549 cells were stimulated with IL-1β, TNF-α, and IL-6 (each at 10 ng/ml) to mimic an inflammatory microenvironment. Metabolic status was evaluated by measuring glutamine uptake, α-ketoglutarate (α-KG), and ATP levels. Functional studies employed the glutaminase inhibitor (CB-839), the MYC inhibitor (10058-F4), SLC1A5 small interfering RNA (siSLC1A5-2), a miR-4652-3p mimic, and overexpression plasmids. Molecular interactions were validated using chromatin immunoprecipitation (ChIP), dual-luciferase reporter assays, and RNA pull-down experiment. CCK-8 and Transwell assays were used for the assessment of cell malignant phenotypes. The functional significance of miR-4652-3p was further verified in a xenograft mouse model. RESULTS: miR-4652-3p was downregulated in NSCLC, while MYC and SLC1A5 were upregulated. Inflammatory stimulation enhanced A549 cell proliferation, glutamine uptake, and α-KG/ATP production; these effects were attenuated by CB-839. ChIP and dual-luciferase assays demonstrated that MYC binds the SLC1A5 promoter and activates its transcription. Inhibiting MYC or knocking down SLC1A5 significantly reduced glutamine uptake. Mechanistic analysis revealed that miR-4652-3p directly targets both MYC and SLC1A5 mRNA. miR-4652-3p suppressed glutamine metabolism in NSCLC cells by negatively regulating the MYC/SLC1A5 axis, consequently inhibiting cell growth and tumor progression in a xenograft mouse model, an effect reversed by MYC or SLC1A5 overexpression. CONCLUSIONS: miR-4652-3p blocked the inflammatory microenvironment-induced glutamine metabolic reprogramming by directly suppressing the MYC/SLC1A5 axis, thereby inhibiting NSCLC progression. The miR-4652-3p/MYC/SLC1A5 pathway represents a key regulatory mechanism for metabolic adaptation in NSCLC. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977689/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137549","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":"PTTG1 regulates the TGF-β/Smad pathway to promote the growth and metastasis of gastric cancer cells.","authors":"Dong Wang, Hui Geng, Ziwei Xia, Chenjie Qiu","doi":"10.1186/s41065-026-00647-0","DOIUrl":"10.1186/s41065-026-00647-0","url":null,"abstract":"<p><strong>Background: </strong>Pituitary tumor-transforming gene 1 (PTTG1) has been implicated in multiple malignancies; however, its precise role and regulatory mechanism in gastric cancer remain unclear. This study aimed to determine how PTTG1 regulates cell proliferation, migration, and epithelial-mesenchymal transition (EMT) through the TGF-β/Smad signaling pathway in gastric cancer.</p><p><strong>Methods: </strong>PTTG1 expression in gastric cancer was evaluated using The Cancer Genome Atlas (TCGA) datasets and subsequently validated by western blotting in gastric cancer cell lines. To investigate the biological functions of PTTG1, functional assays including CCK8, colony formation, and Transwell migration and invasion assays were performed following PTTG1 knockdown in SGC-7901 and HGC-27 cells. The effects on EMT were further examined by assessing EMT-related markers by western blotting. Tumorigenic and metastatic potential in vivo was determined using a nude mouse xenograft model. The regulatory influence of PTTG1 on the TGF-β/Smad pathway was analyzed by measuring the expression levels of TGF-β, Smad2, Smad3, and their phosphorylated forms.</p><p><strong>Results: </strong>PTTG1 expression was significantly upregulated in gastric cancer tissues compared with normal gastric mucosa according to TCGA data and validation in cell lines. Silencing PTTG1 in SGC-7901 and HGC-27 cells markedly inhibited proliferation and colony formation (p < 0.01), and suppressed migration and invasion (p < 0.01). Western blotting revealed increased E-cadherin and reduced N-cadherin, α-SMA, and Vimentin expression after PTTG1 knockdown. In vivo, xenograft tumor growth was significantly reduced in nude mice injected with si-PTTG1 cells compared with controls (n = 6 per group; p < 0.05). Mechanistically, PTTG1 depletion attenuated TGF-β, phosphorylated Smad2, and phosphorylated Smad3 levels, indicating inhibition of the TGF-β/Smad pathway.</p><p><strong>Conclusion: </strong>PTTG1 promotes gastric cancer progression by activating the TGF-β/Smad axis to enhance cell proliferation, invasion, and EMT. These findings highlight PTTG1 as a potential diagnostic biomarker and therapeutic target in gastric cancer.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12964809/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146124855","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 GAS6-AS2 regulates vascular smooth muscle cell senescence through the miR-138-5p/AKT1 axis and serves as a diagnostic and prognostic marker for atherosclerosis.","authors":"Wei Dong, Zhencheng Li, Kai Xie, Xiaowen Lai, Zhaochuan Luo, Yun Qiu, Huan Pu, Ying Zhang","doi":"10.1186/s41065-026-00650-5","DOIUrl":"10.1186/s41065-026-00650-5","url":null,"abstract":"<p><strong>Background: </strong>Atherosclerosis (AS) is a leading cause of cardiovascular-related death worldwide. The role and regulatory mechanism of GAS6-AS2 in AS remain unclear.</p><p><strong>Aim: </strong>To investigate the diagnostic/prognostic value of GAS6-AS2 in AS and clarify its molecular mechanism.</p><p><strong>Methods: </strong>107 AS patients and 105 healthy controls were included. The levels of GAS6-AS2, miR-138-5p, and mRNA were measured using RT-qPCR. ROC curve, K-M survival analysis, and Cox regression were performed to evaluate the diagnostic and prognostic value of GAS6-AS2. Bioinformatics prediction and dual-luciferase reporter assay were performed to verify the regulatory axis. Ox-LDL-induced VSMCs were used to construct an AS cell model. The biological functions were assessed using CCK-8, SA-β-Gal, and ELISA.</p><p><strong>Results: </strong>GAS6-AS2 expression was significantly increased in AS patients and in VSMCs treated with ox-LDL, and it showed high diagnostic accuracy and risk prediction for patients with AS. Knockdown of GAS6-AS2 reduced SA-β-Gal-positive cells, downregulated the expression of senescence-related genes and proteins (p16, p21, p53), and decreased the levels of inflammatory factors (IL-6, IL-1β) in ox-LDL-induced VSMCs. Mechanistically, GAS6-AS2 directly bound to miR-138-5p and inhibited its expression, while miR-138-5p targeted AKT1 to suppress its expression. Rescue experiments confirmed that the GAS6-AS2/miR-138-5p/AKT1 axis mediated ox-LDL-induced VSMC senescence and inflammation.</p><p><strong>Conclusions: </strong>GAS6-AS2 is a potential diagnostic and prognostic biomarker for AS. It regulates ox-LDL-induced VSMC senescence and inflammatory response through the sponging of miR-138-5p to upregulate AKT1, providing a novel molecular target for AS treatment.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12958701/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146113054","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":"Yishen Gushu formula exerts osteoprotective effects in OVX-Induced PMOP rats: role of ferroptosis Inhibition and iron metabolism correction.","authors":"Bo Jin, Hao Zeng, ZhiFeng Wei, YongJin Li, XiaoYun Zhang","doi":"10.1186/s41065-026-00642-5","DOIUrl":"10.1186/s41065-026-00642-5","url":null,"abstract":"<p><p>BACKGROUND: Postmenopausal osteoporosis (PMOP) is a common bone disease among middle-aged and elderly women. Ferroptosis, a form of programmed cell death, plays a crucial role in the regulation of bone metabolism. Yishen Gushu Formula (YSGSF), a traditional Chinese medicine (TCM) compound, has clinical potential for treating PMOP, yet its specific mechanism of action remains unclear. OBJECTIVE: This study aims to investigate the specific mechanism by which YSGSF treats PMOP by inhibiting ferroptosis through mediating the NCOA4/GPX4 pathway. METHODS: The rat PMOP model was established by OVX and treated with YSGSF for 12 consecutive weeks. HE staining and micro-CT were used to examine bone tissue morphology and structure. Serum levels of E2, PINP, and β-CTX were measured by ELISA. RNA-seq analysis was performed to explore the potential mechanism of YSGSF. Oxidative stress markers (ROS, MDA, SOD, GSH, FE) in rat serum were determined. The regulatory effects of YSGSF on NCOA4, FTH1, GPX4, and SLC7A11 were evaluated by IHC and qRT-PCR. Erastin was used in vitro to induce ferroptosis in ROS17/28 osteoblasts, with cell viability and ferroptosis-related protein levels detected by CCK8 and Western blotting. RESULTS: YSGSF improved bone metabolism in OVX rats, alleviated osteoporotic morphological changes, promoted the overall structural recovery of trabecular bone, and increased bone density. RNA-seq suggested that YSGSF may exert its therapeutic effect on PMOP by inhibiting ferroptosis. Subsequent results indicated that YSGSF improved iron metabolism in bone tissue and suppressed iron-dependent oxidative damage. It reduced serum iron ion accumulation and inhibited the production of ROS and MDA. IHC and qRT-PCR confirmed that YSGSF suppressed the expression of NCOA4, upregulated FTH1, and further increased the expression levels of GPX4 and SLC7A11. In vitro cell experiments demonstrated that YSGSF ameliorates Erastin-induced ferroptosis in osteoblasts, improving the expression of related proteins and cell viability. CONCLUSION: YSGSF ameliorates OVX-induced PMOP, potentially by inhibiting osteoblast ferroptosis through modulation of the NCOA4/GPX4 pathway. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12924249/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146118696","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":"Multi-omics integration in deciphering non-small cell lung cancer drug resistance: current status, challenges, and future prospects.","authors":"Jidong Miao, Wenqiang Guan, Jing Wang, Huiying Gong, Qian Xie, Yang Gao","doi":"10.1186/s41065-025-00570-w","DOIUrl":"10.1186/s41065-025-00570-w","url":null,"abstract":"<p><p>Lung cancer is the leading cause of cancer-related deaths globally. Non-small cell lung cancer (NSCLC) accounts for approximately 85% of all lung cancer cases, and drug resistance severely undermines treatment efficacy. This review summarizes recent advances in elucidating NSCLC drug-resistance mechanisms using multi-omics integration. Multi-omics integration systematically reveals the molecular networks of drug resistance, identifies key biomarkers and targets, and facilitates the screening of high-priority candidates for drug development through experimental validation. Small-molecule inhibitors targeting drug-resistant proteins and multi-omics-guided combination therapies offer strategies to reverse resistance. Future directions involve developing simultaneous multi-omics detection technologies, leveraging artificial intelligence for intelligent data analysis, establishing standardized frameworks for data sharing, and implementing personalized medicine based on multi-omics to improve patient prognosis.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":"5"},"PeriodicalIF":2.6,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12862923/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100187","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":"Unraveling the complexities of caffeine: metabolism, genetics, evolution, and health.","authors":"Xinyi Liu, Shuhua Xu","doi":"10.1186/s41065-026-00648-z","DOIUrl":"10.1186/s41065-026-00648-z","url":null,"abstract":"<p><p>Caffeine (1,3,7-trimethylxanthine) is the most widely consumed psychoactive substance globally, yet individuals differ strikingly in their physiological and health responses. These differences arise from the combined effects of genetic variation, evolutionary history, lifestyle exposures, and cultural practices. In this review, we synthesize current knowledge on the pharmacokinetics of caffeine, emphasizing the central role of the hepatic enzyme CYP1A2 and its transcriptional regulator AHR in determining metabolic rate. We summarize functional polymorphisms, haplotypes, and genome-wide association signals that underlie the spectrum from slow to rapid metabolizers, and integrate population-genetic and ancient DNA evidence to reveal how evolutionary pressures have shaped global patterns of caffeine tolerance. We further examine non-genetic modulators—including smoking, pregnancy, diet, and commonly prescribed medications—that dynamically influence CYP1A2 activity. Finally, we discuss how genetic variation interacts with coffee and tea’s diverse bioactive components to influence cardiovascular, neurological, and metabolic outcomes. By uniting pharmacogenomics, evolutionary genetics, and epidemiology, this review highlights the need for personalized caffeine intake recommendations that account for genetic background, beverage preparation methods, and individual health status.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12954933/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100135","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 energy metabolism-related genes in diabetic kidney disease through integrated bioinformatics and in vivo analysis.","authors":"Hui Jiang, Ming-Hui Geng, Yue-Mei Zhan, Jin-Feng Shen, Fu-Zhen Wang, Sen-Qing Lin, Zhe Hong, Chun-Hua Guo, Jin-Xiu Deng, Sen-Chao Wu","doi":"10.1186/s41065-026-00632-7","DOIUrl":"10.1186/s41065-026-00632-7","url":null,"abstract":"<p><strong>Background: </strong>The primary renal complication of diabetes mellitus is diabetic kidney disease (DKD). The precise pathogenic mechanisms of DKD remain poorly elucidated. The aim of this study was to identify potential energy metabolism-related genes associated with DKD.</p><p><strong>Methods: </strong>The GSE30529 and GSE30528 datasets were retrieved from the Gene Expression Omnibus, and energy metabolism-related genes were obtained from the GeneCards database. Differentially expressed genes (DEGs) between DKD and control groups were analyzed. The biological functions and signaling pathways of these DEGs were evaluated using Gene Ontology (GO), the Kyoto Encyclopedia of Genes and Genomes (KEGG), and gene set enrichment analysis (GSEA). The diagnostic performance of hub genes for DKD was assessed using receiver operating characteristic (ROC) curve analysis. Expression levels of five significant energy metabolism-related genes were validated through immunohistochemistry. The Nephroseq V5 tool was used to evaluate gene expression in DKD and to determine correlations between gene expression and renal function in patients with DKD.</p><p><strong>Results: </strong>A total of 17 energy metabolism-related DEGs were identified. Five hub genes-ALB, IGF1, CD36, LPL, and UCP2-were identified. Among these, CD36 and LPL demonstrated relatively high diagnostic accuracy for DKD. The findings suggest that CD36, IGF1, LPL, and UCP2 may serve as potential biomarkers for DKD.</p><p><strong>Conclusions: </strong>The genes CD36, IGF1, LPL, and UCP2 represent potential energy metabolism-related biomarkers with possible applications in the diagnosis and treatment of DKD.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12924410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146062482","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":"Ginsenoside Rg1 delays the senescence of adipose-derived stem cells: network pharmacology and experimental validation.","authors":"Yuan Fang, Chenghong Mou, Xinlang Yu, Jiakang Zhang, Weina Zhu, Chungen Zhou, Bin Jiang, Yanni Chen","doi":"10.1186/s41065-026-00646-1","DOIUrl":"10.1186/s41065-026-00646-1","url":null,"abstract":"<p><p>BACKGROUND: Mesenchymal stem cell (MSC) senescence limits their therapeutic potential. Adipose-derived stem cells (ADSCs), though easily accessible, are prone to senescence under oxidative or inflammatory stress. Ginsenoside Rg1, with antioxidant and anti-inflammatory properties, may counteract this process. This study investigates whether Rg1 can alleviate ADSC senescence and its underlying mechanisms. METHODS: To explore the molecular mechanisms by which Ginsenoside Rg1 mitigates ADSC senescence, network pharmacology and molecular docking were applied to identify potential signaling pathways and targets. Cell viability was measured using the Cell Counting Kit-8 (CCK-8) assay to select the optimal modeling concentration. Flow cytometry was used to analyze cell cycle distribution and immune-related marker expression in ADSCs. Reverse transcription quantitative PCR (RT-qPCR) quantified stemness- and senescence-related gene expression. Immunofluorescence (IF) staining assessed senescence-associated protein levels. Western blotting (WB) was performed to examine key proteins in the PI3K/AKT signaling pathway. RESULTS: Network pharmacology identified 22 aging-associated genes targeted by Rg1, with AKT1 emerging as a central hub protein exhibiting high binding affinity. In hydrogen peroxide (H₂O₂)-induced senescence model, Rg1 treatment significantly enhanced cell viability and stemness, while reducing senescence markers p16 and p21. Furthermore, Rg1 attenuated DNA damage, decreased pro-inflammatory cytokine expression, and restored telomere length. It also promoted cell cycle progression and upregulated immune checkpoint proteins CD59 and CD73. Mechanistic analysis revealed that these anti-senescent effects are mediated via activation of the PI3K/AKT signaling pathway. CONCLUSION: Rg1 effectively attenuates ADSC senescence by activating the PI3K/AKT signaling pathway, promoting cell cycle progression and enhancing immune evasion capacity. This reveals a novel anti-aging mechanism and offers new insights for MSC-based regenerative therapies, while also providing modern evidence supporting the traditional Jing-Qi theory. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":"31"},"PeriodicalIF":2.6,"publicationDate":"2026-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918114/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146062493","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}