Biochemical Genetics最新文献

{"title":"Association of HindIII Polymorphism of the Lipoprotein Lipase (LPL) Gene (rs320) and Plasma Metabolic Parameters in a Nigerian Population.","authors":"Joseph O Faleti, Holiness S A Olasore, Matthew O Olawale, Abdullahi A Murtala, Taiwo O Banjo, Miriam N Igwo-Ezikpe","doi":"10.1007/s10528-025-11039-w","DOIUrl":"https://doi.org/10.1007/s10528-025-11039-w","url":null,"abstract":"<p><p>Genetic variations in the lipoprotein lipase (LPL) gene including the HindIII polymorphism (rs320) have been reported to modify fat metabolism, adiposity, and body weight. However, little attention has been given to the African population. The present study aimed to investigate the relationship between the rs320 gene polymorphism and a number of metabolic and anthropometric parameters in a sample of the Nigerian population. We recruited 236 participants for the study. The participants were required to sign informed consent forms after which information related to their calorie intake and utilization as well as anthropometric measurements were recorded. Plasma metabolic parameters were subsequently determined using an autoanalyzer. Genotyping for HindIII polymorphism was performed using the PCR-RFLP method. The frequencies (n) of T and G alleles were 0.841 (397) and 0.158 (75), while the frequencies (n) of TT, TG, and GG were 0.691(163), 0.301(71), and 0.01(2), respectively. The population was not in Hardy-Weinberg equilibrium (χ² = 3.717, df = 1, p = 0.841). The anthropometric parameters, the fasting blood glucose, and low-density lipoprotein cholesterol showed no association with the alleles, while plasma high-density lipoprotein cholesterol and total cholesterol were significantly higher among the G allele carriers. However, triglyceride and total protein were significantly higher among the non-G allele carriers. The LPL HindIII gene polymorphism is associated with changes in plasma lipid profile in a sample of the Nigerian population.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143078290","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing Chemokine Signaling Pathways and Hub Genes in Calcium Oxalate-Induced Kidney Stone Formation: Insights from Rodent Models.","authors":"Boqiang Wang, Zhenkun Tan, Wusheng She, Xiang Wang, Xiaofeng Guan, Zhiwei Tao, Fuyou Guo, Hua Xu, Yaoliang Deng","doi":"10.1007/s10528-025-11036-z","DOIUrl":"https://doi.org/10.1007/s10528-025-11036-z","url":null,"abstract":"<p><p>The predominant component of kidney stone is calcium oxalate monohydrate (COM), a fact widely acknowledged. Although rodent models are frequently used to induce calcium oxalate (CaOx) crystallization, further exploration of Randall's plaques (RPs) in these models is still needed. We first selected the GSE89028 and GSE75542 datasets from the Gene Expression Omnibus (GEO) database to identify commonly differentially expressed genes (co-DEGs). Based on co-DEGs, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to identify significantly enriched pathways. Additionally, we performed Gene Set Enrichment Analysis (GSEA) to validate the enriched pathways. In order to identify hub genes, we established a network of protein-protein interactions (PPI). Finally, we conducted real-time PCR and Western blot to validate the findings from the bioinformatics analysis. We selected 28 co-DEGs from two datasets. The enrichment analysis using GO, KEGG, and GSEA revealed significant enrichment of chemokine-related signaling pathways. The histogram analysis showed that three chemokine factor-related genes were involved in multiple pathways. We used Cytohubba to confirm the presence of three hub genes. Subsequently, analysis of external datasets and quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot demonstrated significant upregulation of CCL2, CXCL1, and CXCL2 in HK-2 cells following CaOx treatment compared to the control group (p < 0.05). Our study demonstrated that upon stimulation by CaOx, renal tubular epithelial cells release chemokines, including CCL2, CXCL1, and CXCL2. This release of chemokines is accompanied by the activation of signaling pathways such as TNF and IL-17. These findings may provide new directions for future research on Kidney Stone Disease.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143073379","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Computational Elucidation of Hub Genes and Pathways Correlated with the Development of 5-Fluorouracil Resistance in HCT 116 Colorectal Carcinoma Cell Line.","authors":"Chun Hoe Tan, Siew Huah Lim, Kae Shin Sim","doi":"10.1007/s10528-025-11041-2","DOIUrl":"https://doi.org/10.1007/s10528-025-11041-2","url":null,"abstract":"<p><p>Colorectal cancer (CRC) is the third most deadly cancer diagnosed in both men and women. 5-Fluorouracil (5-FU) treatment frequently causes the CRC cells to become chemoresistance, which has a negative impact on prognosis. Using bioinformatic techniques, this work describes important genes and biological pathways linked to 5-FU resistance in CRC cells. In our studies, a 5-FU-resistant HCT 116 cell line exhibiting elevated TYMS was created and validated using various tests. Bioinformatic studies were conducted to determine which differentially expressed genes (DEGs) were responsible for the establishment of 5-FU resistance in the same cell line. After screening 3949 DEGs from the two public datasets (GSE196900 and GSE153412), 471 overlapping DEGs in 5-FU-resistant HCT 116 cells were chosen. These overlapping DEGs were used to build the PPI network, and a major cluster module containing 21 genes was found. Subsequently, using three topological analysis algorithms, 10 hub genes were identified, which included HLA-DRA, HLA-DRB1, CXCR4, MMP9, CDH1, SMAD3, VIM, SYK, ZEB1, and SELL. Their roles were ascertained by utilizing Gene Ontology keywords and pathway enrichment studies. Our results also demonstrated that the miRNA and transcription factors (TFs) that had the strongest connection with the hub genes were hsa-mir-26a-5p, hsa-mir-30a-5p, RELA, and NFKB1. Ultimately, 84 FDA-approved drugs that target those hub genes were found to potentially treat 5-FU resistance CRC. Our research's findings increase our understanding of the fundamental factors that contribute to the prevalence of 5-FU resistance CRC, which could ultimately assist in the identification of valuable malignancy biomarkers and targeted treatment approaches based on key regulatory pathways.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143062977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Relationship Between Differential Expression of Non-coding RNAs (TP53TG1, LINC00342, MALAT1, DNM3OS, miR-126-3p, miR-200a-3p, miR-18a-5p) and Protein-Coding Genes (PTEN, FOXO3) and Risk of Idiopathic Pulmonary Fibrosis.","authors":"Gulnaz F Korytina, Vitaly A Markelov, Irshat A Gibadullin, Shamil R Zulkarneev, Timur R Nasibullin, Rustem H Zulkarneev, Arthur M Avzaletdinov, Sergey N Avdeev, Naufal Sh Zagidullin","doi":"10.1007/s10528-024-11012-z","DOIUrl":"https://doi.org/10.1007/s10528-024-11012-z","url":null,"abstract":"<p><p>Idiopathic pulmonary fibrosis (IPF) is a rapidly progressive interstitial lung disease of unknown pathogenesis with no effective treatment currently available. Given the regulatory roles of lncRNAs (TP53TG1, LINC00342, H19, MALAT1, DNM3OS, MEG3), miRNAs (miR-218-5p, miR-126-3p, miR-200a-3p, miR-18a-5p, miR-29a-3p), and their target protein-coding genes (PTEN, TGFB2, FOXO3, KEAP1) in the TGF-β/SMAD3, Wnt/β-catenin, focal adhesion, and PI3K/AKT signaling pathways, we investigated the expression levels of selected genes in peripheral blood mononuclear cells (PBMCs) and lung tissue from patients with IPF. Lung tissue and blood samples were collected from 33 newly diagnosed, treatment-naive patients and 70 healthy controls. Gene expression levels were analyzed by RT-qPCR. TaqMan assays and TaqMan MicroRNA assay were employed to quantify the expression of target lncRNAs, mRNAs, and miRNAs. Our study identified significant differential expression in PBMCs from IPF patients compared to healthy controls, including lncRNAs MALAT1 (Fold Change = 3.809, P = 0.0001), TP53TG1 (Fold Change = 0.4261, P = 0.0021), and LINC00342 (Fold Change = 1.837, P = 0.0448); miRNAs miR-126-3p (Fold Change = 0.102, P = 0.0028), miR-200a-3p (Fold Change = 0.442, P = 0.0055), and miR-18a-5p (Fold Change = 0.154, P = 0.0034); and mRNAs FOXO3 (Fold Change = 4.604, P = 0.0032) and PTEN (Fold Change = 2.22, P = 0.0011). In lung tissue from IPF patients, significant expression changes were observed in TP53TG1 (Fold Change = 0.2091, P = 0.0305) and DNM3OS (Fold Change = 4.759, P = 0.05). Combined analysis of PBMCs expression levels for TP53TG1, MALAT1, miRNA miR-126-3p, and PTEN distinguished IPF patients from healthy controls with an AUC = 0.971, sensitivity = 0.80, and specificity = 0.955 (P = 6 × 10^-8). These findings suggest a potential involvement of the identified ncRNAs and mRNAs in IPF pathogenesis. However, additional functional validation studies are needed to elucidate the precise molecular mechanisms by which these lncRNAs, miRNAs, and their targets contribute to PF.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143062984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic Control of Hyperuricemia and Gout by Gene Writer DNMT1 and RNA Editor ADAR1: Mechanism of Gout and Amyloid Dissolution in Down Syndrome.","authors":"Suresh C Tyagi, Irina Smolenkova, Yuting Zheng, Mahavir Singh","doi":"10.1007/s10528-025-11038-x","DOIUrl":"https://doi.org/10.1007/s10528-025-11038-x","url":null,"abstract":"<p><p>Although DNA methyltransferase 1 (DNMT1) and RNA editor ADAR triplications exist in Down syndrome (DS), their specific roles remain unclear. DNMT methylates DNA, yielding S-adenosine homocysteine (SAH), subsequently converted to homocysteine (Hcy) and adenosine by S-adenosine homocysteine (Hcy) hydrolase (SAHH). ADAR converts adenosine to inosine and uric acid. We hypothesized that targeting epigenetic regulators and RNA editor, and inhibiting Hcy and adenosine, could alleviate DS phenotype including the congenital heart disease (CHD). DS and wild-type mice were treated with epigallocatechin gallate (EG), inhibitor of Hcy, and adenosine. Specific substrate gel zymography identified matrix metalloproteinases (MMPs)/A Disintegrin and Metalloproteinase with Thrombospondin motifs (ADAMTS) activities and MMP12/ADAMTS12 and MMP13/ADAMTS13 levels were assessed via gel zymography. Cardiac levels of DNMT1, ADAR, tissue inhibitor of metalloproteinase 1 (TIMP1), SAHH, and ten-eleven translocator (TET2), along with hydroxymethylation (a gene eraser), were measured. Calcium urate deposits in heart tissue suggested gout mechanism in DS. Robust amyloid fibers in DS mouse brain cortex were most likely dissolved by ADAMTS as its levels were elevated in tissues, with a corresponding decrease in TIMP1 in the EG group. It appears that triplication of down syndrome cell adhesion molecule (DSCAM) and cell adhesion molecule 1 (CAM1) fragment also help dissolve amyloid fibers, thus suggesting ADAMTS13/TIMP1 ratio could predict plaque dissolution. Our results indicate that cystathionine-β synthase (CBS) inhibitor as a potential therapy for amyloid dissolution.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143062981","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNIP1 Impacts Prognosis by Modulating the Immune Microenvironment in BRCA.","authors":"Dong Liao, Wu Liu, Yunhui Jiang, Ping Zhao, Yun Yao","doi":"10.1007/s10528-025-11034-1","DOIUrl":"https://doi.org/10.1007/s10528-025-11034-1","url":null,"abstract":"<p><p>Breast invasive carcinoma (BRCA) affects women worldwide, and despite advancements in diagnosis, prevention, and treatment, outcomes remain suboptimal. TNIP1, a novel target involved in multiple immune signaling pathways, influences tumor development and survival. However, the connection between BRCA and TNIP1 remains unclear. Analysis of data from the TCGA, GEO, Sangerbox, and Ualcan databases revealed that TNIP1 is underexpressed in BRCA tissues. This finding was corroborated by RT-PCR and immunohistochemistry. Furthermore, data from the TCGA and GEPIA2 databases, along with Sangerbox, identified TNIP1 as a marker of poor prognosis in BRCA patients. TNIP1 expression shows significant positive correlations with the BRCA Tumor Microenvironment (TME) StromalScore (R = 0.22), ImmuneScore (R = 0.25), and ESTIMATEScore (R = 0.27). Various algorithms have demonstrated a strong association between TNIP1 expression and BRCA tumor-infiltrating immune cells (TIICs). Further analysis using EPIC, TIMER, MCPCounter, QUANTISEQ, xCell, and other computational tools revealed that elevated TNIP1 expression is significantly associated with increased immune cell scores. TNIP1 expression in BRCA tumor tissues also shows a strong correlation with immune checkpoint markers. Data from the HAP database indicate that TNIP1 expression is predominantly involved in the normal skin microenvironment. Subsequent analysis using the TISCH platform with the BRCA single-cell dataset demonstrated that TNIP1 exhibits higher expression levels in immune cells compared to non-immune cells in BRCA patients. This expression is significantly positively correlated with inflammation (R = 0.25) and differentiation (R = 0.28) within the TME, while showing negative correlations with BRCA stemness (R = - 0.34) and invasion (R = - 0.22). Consequently, TNIP1 is proposed as a potential prognostic marker and therapeutic target for BRCA.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143051237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Angiotensin-Converting Enzyme 2 Enhances Autophagy via the Consumption of miR-326 in a Mouse Model of Acute Lung Injury.","authors":"Xingsheng Lin, Fengying Gao","doi":"10.1007/s10528-025-11040-3","DOIUrl":"https://doi.org/10.1007/s10528-025-11040-3","url":null,"abstract":"<p><p>Angiotensin-converting enzyme 2 (ACE2) has been reported to exert a protective effect in acute lung injury (ALI), though its underlying mechanism remains incompletely understood. In this study, ACE2 expression was found to be upregulated in a mouse model of ALI induced by lipopolysaccharide (LPS) injection. ACE2 knockdown modulated the severity of ALI, the extent of autophagy, and the mTOR pathway in this model. ACE2 regulated liver kinase B1 (LKB1) gene expression by sequestering miR-326, thereby alleviating ALI severity through enhanced autophagy. In cell-based experiments, miR-326 was shown to regulate ACE2 and LKB1 expression and autophagy. Overexpression of ACE2 disrupted miR-326's regulatory effect on LKB1, suggesting that LKB1 may function as an endogenous sponge for miR-326. These findings imply that elevated ACE2 expression in lung could play enhance the autophagy via the consumption of miR-326.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNAs' Significance in Retinoblastoma Diagnosis and Treatment: The Little Heroes.","authors":"Maryam Zamani Sani, Mohammad Mirzaei, Ali Mota, Jamal Mohammadian, Elmira Aboutalebi Vand Beilankouhi, Mohammad Rahmati","doi":"10.1007/s10528-024-10976-2","DOIUrl":"https://doi.org/10.1007/s10528-024-10976-2","url":null,"abstract":"<p><p>One in 16, 000 live births is affected by the retinal tumor RB (retinoblastoma), which is frequently found in a child's early years. Both of the RB1 alleles that have been locally mutated in the affected retina are present in 60 percent of cases. Retinoblastoma (RB) can be detected using a variety of techniques, including imaging of the brain and orbits, eye examinations under anesthesia (EUAs), and the discovery of cell-free tumor DNA in samples of aqueous humor or plasma. In addition to the conventional surgical, chemotherapy, and radiotherapy approaches to treating retinoblastoma, new approaches have also been developed. Oncogenes, genes of tumor suppressors, and other molecular elements involved in cell growth and division interact complexly during the pathogenesis of retinoblastoma. The development of new therapies depends on comprehending the function of these molecular components. As a small class of non-coding RNAs capable of altering gene expression, microRNAs (miRNA) are understood to represent potential targets for the treatment of cancer. This study aimed to describe the changes in microRNA expression in some types of cancer, with a particular focus on retinoblastoma.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143035870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Haplotypes of Chloroquine Resistance Marker Genes Among Uncomplicated Malaria Cases in Lagos, Nigeria.","authors":"Uche Thecla Igbasi, Wellington Aghoghavia Oyibo, Jun-Hu Chen, Hong Quan, Sunday Aremu Omilabu, Shen-Bo Chen, Hai-Mo Shen, Xiao-Nong Zhou","doi":"10.1007/s10528-025-11022-5","DOIUrl":"https://doi.org/10.1007/s10528-025-11022-5","url":null,"abstract":"<p><p>Drug resistance resulting from mutations in Plasmodium falciparum, that caused the failure of previously effective malaria drugs, has continued to threaten the global malaria elimination goal. This study describes the profiles of P. falciparum chloroquine resistance transporter (Pfcrt) and P. falciparum multidrug resistance 1 (Pfmdr1), the genetic markers associated with 4-aminoquinoline resistance, among P. falciparum isolates from Lagos, Nigeria. Genomic DNA was extracted from the dried blood spot samples obtained from individuals with microscopically confirmed P. falciparum infection in health facilities and communities in Lagos State, Nigeria. The DNA was amplified using nested polymerase chain reaction, and sequence analysis was performed to identify single nucleotide polymorphisms in the pfcrt and pfmdr1 genes. The study showed that 82.4% (178) of the isolates had pfmdr1 wild-type, while mutations were observed at codons N86Y (11.6%) and D1246Y (3.2%). Other mutations seen were at codons Y23S (0.5%), E130K (2.3%), and S149P (0.5%). 30.8% (64) of the isolates had pfcrt wild-type (CVMNK), while 62.0% (129) had CVIET (mutant) haplotype. Other pfcrt haplotypes detected include; CVIDT (1.9%); CVMDT (1.4%); CVIKT (1.0%); CVINT (0.5%); CVMET (0.5%); CVMKT (0.5%); CVMNT (1.0%); and CVMEK (0.5%). The findings underscore the presence of uncommon pfcrt haplotypes and a high prevalence of drug-resistant pfcrt haplotypes (CVIET), alongside a high prevalence of wild-type pfmdr in Lagos. This study highlights the need for ongoing surveillance of these genetic markers to provide data that can inform decisions on malaria case management and preserve the efficacy of artemisinin combination therapies (ACTs) in Nigeria.</p>","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998118","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Curcumol Attenuates Portal Hypertension and Collateral Shunting Via Inhibition of Extrahepatic Angiogenesis in Cirrhotic Rats.","authors":"Xinyuan Wang, Juan Li, Jiao Nong, Xin Deng, Yiping Chen, Peibin Wu, Xiabing Huang","doi":"10.1007/s10528-025-11023-4","DOIUrl":"https://doi.org/10.1007/s10528-025-11023-4","url":null,"abstract":"","PeriodicalId":482,"journal":{"name":"Biochemical Genetics","volume":" ","pages":""},"PeriodicalIF":2.1,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142998035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}