Hereditas最新文献

{"title":"Integrated bioinformatics analysis and experimental validation reveal Pevonedistat as a promising therapeutic agent modulating the CRL4-DTL-p21/p53 axis in nasopharyngeal carcinoma.","authors":"Cong-Chao Jia, Zhen-Yi Li, Wei-Hua Jia, Cheng-Tao Jiang","doi":"10.1186/s41065-026-00661-2","DOIUrl":"10.1186/s41065-026-00661-2","url":null,"abstract":"<p><p>BACKGROUND: Nasopharyngeal carcinoma (NPC) continues to represent a significant therapeutic challenge. Despite the substantial success of radiotherapy, chemotherapy, and immunotherapy, their effectiveness remains limited in recurrent or advanced NPC. Hence, the urgent identification of new molecular targets and effective therapeutic agents is critically required. METHODS: Bulk and single-cell transcriptomic data were analyzed using bioinformatics approaches, and machine learning algorithms were employed to screen for hub genes in NPC. Functional validation of hub genes was performed through loss-of-function assays. Potential therapeutic agents were identified through molecular docking and subsequently evaluated for anti-NPC efficacy using both in vitro NPC cell line models and in vivo patient-derived xenograft (PDX) models. RESULTS: Bioinformatics analyses revealed DTL as a central gene with critical diagnostic and prognostic significance. Knockdown of DTL led to cell cycle arrest and apoptosis through stabilization of p21 and p53. Pevonedistat markedly inhibited DTL activity, recapitulating the effects of DTL knockdown. In vitro studies showed that Pevonedistat suppressed NPC cell proliferation, while in PDX models it significantly reduced tumor burden. Collectively, the data establish DTL as a key oncogenic driver in NPC and highlight Pevonedistat as a promising therapeutic candidate. CONCLUSION: Our work presents an integrated framework for target identification and therapeutic development in NPC. These findings deepen our understanding of NPC biology and highlight that Pevonedistat suppresses cell proliferation and tumor growth of NPC via the CRL4-DTL-p21/p53 axis. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13081564/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147372520","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":"Perillaldehyde inhibits oxidative stress, NLRP3-mediated inflammation and fibrosis in diabetic nephropathy through regulating HMOX1.","authors":"Wen Hao, Chunhua Liu, Jing Feng, Zhanliang Ren","doi":"10.1186/s41065-026-00657-y","DOIUrl":"10.1186/s41065-026-00657-y","url":null,"abstract":"<p><p>Diabetic nephropathy (DN) is a frequently occurred complication of diabetes mellitus (DM) worldwide. Perillaldehyde is a natural terpenoid compound exerted beneficial effects on diabetic cardiomyopathy (DCM), which is another important part of DM complication. However, the effect of perillaldehyde on DN has not been reported. In the present study, we demonstrated that perillaldehyde prevented ROS-driven oxidative stress, with decreased ROS and MDA levels and increased GSH level in high glucose (HG)-treated HK-2 cells. Perillaldehyde also reversed HG-induced NLRP3-mediated inflammation and fibrosis in HK-2 cells, as evidenced by decreased pro-inflammatory cytokines and fibrogenic factors. Furthermore, we observed that perillaldehyde directly targeted HMOX1 and regulated its expression in HK-2 cells. Knockdown of HMOX1 prevented the effects of perillaldehyde on HG-treated HK-2 cells, implying that perillaldehyde exerted its effects via regulating HMOX1. In a high fat diet (HFD)/streptozocin (STZ) mouse model, perillaldehyde also exerted renoprotective, antioxidant, anti-inflammatory and anti-fibrotic activities. In conclusion, our study clearly demonstrated the beneficial effects of perillaldehyde on DN both in vivo and in vitro, which indicated that perillaldehyde might serve as a potential application in treating or preventing DN.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13077860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147369518","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-3913-3p promoted the progression of lung adenocarcinoma by regulating STX3 expression.","authors":"Yu Wang, Lin Shen, Ruijie Cao, Hao Xu, Zhong Guo, Yuxing Chen, Dan Wang","doi":"10.1186/s41065-026-00654-1","DOIUrl":"10.1186/s41065-026-00654-1","url":null,"abstract":"<p><p>BACKGROUND: The prognostic relevance and operational pathways of miR-3913-3p during disease advancement are not entirely clarified. This research intends to thoroughly assess the clinical importance and mechanistic contributions of miR-3913-3p within lung adenocarcinoma (LUAD) contexts. METHODS: Relationships linking miR-3913-3p abundance with five-year survival rates were examined through Kaplan-Meier methodology, while prognostic strength was determined by multivariate Cox regression modeling. Quantification of miR-3913-3p and STX3 in clinical specimens and cellular models was accomplished via RT-qPCR. Functional impacts on LUAD cells and regulatory interactions with target genes were validated through cell transfection, CCK-8 assays, Transwell migration/invasion assays, and dual-luciferase reporter assays. RESULTS: miR-3913-3p expression was significantly elevated in LUAD tissues compared to matched non-tumor tissues. High miR-3913-3p expression was significantly correlated with poor tumor differentiation, advanced TNM stage, and lymph node metastasis (p < 0.05). Multivariate Cox analysis identified high miR-3913-3p expression as a predictor of poor prognosis (HR = 2.450, 95% CI: 1.014–5.920, p = 0.046). Functionally, miR-3913-3p mimic enhanced the proliferative, migratory, and invasive capacities of LUAD cells, whereas miR-3913-3p inhibitor suppressed these malignant behaviors. Notably, co-transfection with si-STX3 rescued the inhibitory effects induced by the miR-3913-3p inhibitor. Mechanistically, dual-luciferase reporter assays confirmed that miR-3913-3p directly binds to the 3’untranslated region (3’UTR) of STX3, leading to its functional suppression. CONCLUSION: This study demonstrates the existence of a regulatory miR-3913-3p/STX3 axis in LUAD. miR-3913-3p likely promotes the proliferation, migration, and invasion of LUAD cells by targeting STX3, implicating this axis in LUAD pathogenesis. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067435/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348252","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":"Exploring 14-3-3ζ: insights into its role in cancer mechanisms and future therapeutic applications.","authors":"Husni Farah, Munthar Kadhim-Abosaoda, Hayjaa Mohaisen-Mousa, S Renuka Jyothi, Priya Priyadarshini-Nayak, Bethanney Janney-J, Gurjant Singh, Ashish Singh-Chauhan, Manoj Kumar-Mishra","doi":"10.1186/s41065-026-00658-x","DOIUrl":"10.1186/s41065-026-00658-x","url":null,"abstract":"<p><p>14–3-3ζ is becoming an important marker and possible treatment target because many studies link it with cancer recurrence and resistance to chemotherapy. When cancer cells make too much 14–3-3ζ, they tend to survive better, especially under stressful conditions, and they can grow even without attachment, which is usually a sign of more aggressive behavior. On the other hand, when the level of 14–3-3ζ is lowered, tumors grow slower and the cells become more sensitive to different anticancer drugs. In clinical settings high 14–3-3ζ can work as prognostic biomarker, helping to identify patients whose tumors might not respond fit to standard treatments, allowing doctors to think about more personalized therapy options. This protein also interacts with several cancer-related pathways for example working together with HER2, which can push tumors to become more invasive, and harder to treat. Many cancers show amplification of the 14–3-3ζ gene and this usually correlates with worse outcomes for patients. Even though scientists are still figuring out how directly target 14–3-3ζ, a lot of studies suggest that stopping this protein or blocking the signals it activates might make cancer cells respond better in chemo and slow the tumor from getting worse [14]. So overall, going after 14–3-3ζ looks like the pretty promising approach for dealing with therapy resistance, and it could maybe help improve patient outcomes in the future.</p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13067609/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147348270","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":"Pan-cancer analysis of PDZK1IP1 reveals its role in tumorigenesis and tumor immunity: focused validation in thyroid carcinoma.","authors":"Chenchen Geng, Xiaoqian Gao, Yali Le, Shuzhen Zhu, Guanghui Zhao, Ping Zhang","doi":"10.1186/s41065-026-00662-1","DOIUrl":"10.1186/s41065-026-00662-1","url":null,"abstract":"<p><p>BACKGROUND: PDZK1IP1 is a membrane protein linked to inflammation and cancer, but its role in the tumor immune microenvironment is poorly understood. This study systematically investigated the oncogenic and immunological functions of PDZK1IP1 via a pan-cancer analysis, with experimental validation in thyroid carcinoma (THCA). METHODS: We conducted a comprehensive bioinformatic analysis of PDZK1IP1 using publicly available platforms (TIMER, GEPIA, c-BioPortal, TISIDB, SangerBox) to examine its expression, diagnostic potential, prognostic relevance, and correlation with key immune features, including immune checkpoint genes, tumor mutational burden, neoantigen load, tumor stemness, and immune cell infiltration. Findings were validated in a THCA cohort using RT-PCR and immunohistochemistry. RESULTS: PDZK1IP1 was overexpressed in multiple cancers, showed significant diagnostic potential, and was a context-dependent prognostic marker, correlating with poor relapse-free survival in THCA. Its expression was strongly associated with tumor mutational burden, neoantigen load, tumor stemness, and the infiltration of various immune cells (particularly neutrophils) across multiple cancers. These findings were corroborated in THCA, in which PDZK1IP1 expression correlated with the infiltration of five distinct immune cell types. Functional enrichment analysis confirmed an association with neutrophil activation pathways. CONCLUSIONS: Our study identified PDZK1IP1 with dual functions, acting as both an oncogene and a modulator of the tumor immune microenvironment. These findings highlight its potential as a prognostic biomarker and therapeutic target for immunotherapy, especially in THCA. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13049858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147316846","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":"Correction: The diagnostic value of miR-340-5p in pediatric ulcerative colitis and its molecular mechanism by targeting MAP3K2 to modulate intestinal epithelial cell dysfunction.","authors":"Fanting Meng, Xianlong Han, Lingxia Ge, Nan Guan","doi":"10.1186/s41065-026-00652-3","DOIUrl":"10.1186/s41065-026-00652-3","url":null,"abstract":"","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":"163 1","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12930794/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147283484","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":"Development and validation of a succinylation-related prognostic model for esophageal squamous cell carcinoma based on multi-omics bioinformatics analysis.","authors":"Beibei Hua, Weiwei Wang, Huijie Huang, Xuezhi Chang, Tao Ye","doi":"10.1186/s41065-026-00653-2","DOIUrl":"10.1186/s41065-026-00653-2","url":null,"abstract":"<p><p>BACKGROUND: Esophageal squamous cell carcinoma (ESCC), an aggressive malignancy with poor prognosis, requires reliable prognostic biomarkers. Protein succinylation, a critical post-translational modification implicated in cancer biology, has not yet been systematically investigated for its prognostic significance in ESCC. METHODS: Transcriptomic data from GSE53624 (n = 119) and The Cancer Genome Atlas (TCGA)-ESCC (n = 95) cohorts were analyzed in this study. Succinylation-related genes (SRGs) were identified via weighted gene co-expression network analysis (WGCNA), a curated SRG set, and differential expression analysis. A prognostic signature was constructed using LASSO Cox regression and validated internally and externally. Immune infiltration was assessed by CIBERSORT/ssGSEA. miRNA-mRNA and protein-protein interactions (PPIs) and drug sensitivity were evaluated. Gene localization was confirmed with single-cell RNA sequencing (scRNA-seq). RESULTS: 41 high-confidence SRGs associated with ESCC were identified. A robust seven-gene prognostic signature (IGFBP3, CMA1, FN1, CTSG, TIMP1, MBL2, and SP5) was established. Patients stratified into high- and low-risk groups exhibited significantly different overall survival (OS) in both the training cohort (GSE53624, P < 0.001) and the validation cohort (TCGA, P = 0.026). The risk score remained an independent prognostic factor and was incorporated into a predictive nomogram. High-risk tumors were characterized by an immunosuppressive tumor microenvironment (TME), with reduced eosinophil and natural killer (NK) cell infiltration and increased monocyte abundance. In addition, signature genes were associated with resistance to multiple anticancer agents. scRNA-seq analysis revealed predominant expression of these genes in malignant cells, fibroblasts, and myeloid cells. CONCLUSION: A novel seven-gene succinylation-related signature was established and validated as an independent prognostic biomarker for ESCC. This signature captures immunosuppressive features of high-risk tumors and may provide a foundation for individualized therapeutic strategies. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015151/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146212986","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":"ZSGSD inhibits colorectal cancer via PI3K/AKT/mTOR pathway: pharmacological and experimental evidence.","authors":"Ting Wu, Jingwen Jiang, Yunfang Zhang, Hui Zhang, Mingquan Fu, Fazhang Chen, Yilin Fan, Huan Yuan, Kaining Wang","doi":"10.1186/s41065-026-00636-3","DOIUrl":"10.1186/s41065-026-00636-3","url":null,"abstract":"<p><p>BACKGROUND: Colorectal cancer (CRC) remains one of the most commonly diagnosed malignancies worldwide and is associated with high recurrence and poor survival outcomes, particularly in its advanced stages. Zi-Shen-Gu-Sui Decoction (ZSGSD), a traditional Chinese medicinal formula, has been clinically applied in CRC treatment and postoperative rehabilitation; however, its pharmacological mechanisms are not yet fully elucidated. This study aimed to explore the anti-CRC efficacy and molecular mechanisms of ZSGSD, with particular attention to the PI3K/AKT/mTOR signaling axis. METHODS: UPLC-Q-Orbitrap HRMS was utilized to characterize the chemical profile of ZSGSD. Network pharmacology was employed to identify key signaling pathways and bioactive compounds, and molecular docking was conducted to predict potential interactions between major constituents and PI3K/AKT/mTOR proteins. A xenograft mouse model of CRC was established to evaluate tumor suppression. Histological staining was used to assess apoptosis, and the expression of PI3K, AKT, and mTOR was quantified via RT-qPCR, Western blotting, and immunofluorescence assays. RESULTS: Sixty compounds were identified in ZSGSD, with flavonoids comprising approximately 50%. Network analysis suggested potential involvement of the PI3K/AKT/mTOR pathway, and docking results indicated favorable predicted binding between key flavonoids (including Genistein, Apigenin, and Naringenin) and proteins within this pathway. In vivo, ZSGSD treatment suppressed tumor growth in a dose-responsive fashion, with tumor inhibition rates ranging from 30.83% to 75.23% (p < 0.05). Histological evaluations revealed reduced nuclear-to-cytoplasmic ratios and enhanced apoptotic activity, as confirmed by TUNEL staining (p < 0.05). Molecular analyses showed a dose-related reduction in PI3K, AKT, and mTOR expression at the transcript and protein levels, indicating that this pathway may be modulated during ZSGSD treatment (p < 0.05). CONCLUSION: ZSGSD demonstrates notable tumor-suppressive and pro-apoptotic effects in a CRC xenograft model. These outcomes appear to be associated with modulation of the PI3K/AKT/mTOR signaling pathway, although further functional studies are required to confirm pathway specificity and clarify causal mechanisms. </p>","PeriodicalId":12862,"journal":{"name":"Hereditas","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13015177/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146201470","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":"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}