BioFactorsPub Date : 2026-07-02DOI: 10.1002/biof.70125
Pengxiao Hou, Zhizhong Liang, Qian Wu
{"title":"Dauriporphine Inhibits the Proliferation, Migration, Angiogenesis, and Glycolysis in Lung Cancer Cells by Repressing PGK1 Expression via CEBPA","authors":"Pengxiao Hou, Zhizhong Liang, Qian Wu","doi":"10.1002/biof.70125","DOIUrl":"10.1002/biof.70125","url":null,"abstract":"<div>\u0000 \u0000 <p>Many anti-cancer agents with therapeutic potential have been discovered in traditional Chinese medicine. Dauriporphine is an alkaloid extracted from <i>Menispermum dauricum DC.</i>, demonstrating anti-cancer properties. However, the precise role of dauriporphine in the treatment of lung cancer and its underlying biological mechanism remains unclear. Dauriporphine addition resulted in reduced proliferation, migration, angiogenesis, and glycolysis in A549 and H1299 cells. Phosphoglycerate kinase 1 (PGK1) was identified as the candidate gene involved in glycolysis and dauriporphine after prediction using public datasets. Dauriporphine administration decreased PGK1 expression, whereas PGK1 overexpression markedly abolished the suppressive effects of dauriporphine. The CCAAT/enhancer binding protein A (CEBPA) was predicted to be the transcription factor of PGK1 using the online QIAGEN. The binding between CEBPA and PGK1 promoter was predicted and verified using Jaspar algorithm and Human TFDB, as well as chromatin immunoprecipitation (ChIP), dual-luciferase reporter assay, and cellular thermal shift assay (CETSA). CEBPA silencing could repress tumor cell malignant behaviors, which could be partially restored by PGK1 overexpression. Moreover, the upregulation of CEBPA diminished the anti-tumor efficacy of dauriporphine. Furthermore, dauriporphine treatment suppressed tumor growth by regulating the CEBPA/PGK1 pathway in nude mice. Overall, the study demonstrated that dauriporphine inhibited proliferation, migration, angiogenesis, and glycolysis in lung cancer cells via the CEBPA/PGK1 pathway, providing a potentially effective therapeutic strategy for lung cancer.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 4","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Targeting the Tumor Immune Ecosystem in Glioblastoma: Challenges and Innovations in Immunotherapy","authors":"Cheng Cheng, Yijue Wang, Yiru Wen, Yaqiang Bai, Yanni Xia, Yue Feng, Zeping Chen","doi":"10.1002/biof.70132","DOIUrl":"https://doi.org/10.1002/biof.70132","url":null,"abstract":"<div>\u0000 \u0000 <p>Glioblastoma (GBM) is the most aggressive primary brain tumor, marked by poor prognosis and resistance to conventional therapies. A critical barrier to effective treatment lies in its highly immunosuppressive and heterogeneous tumor microenvironment (TME), which orchestrates immune evasion and therapeutic failure. Tumor-associated macrophages (TAMs), particularly those with an M2-like phenotype, sustain GBM proliferation, angiogenesis, and stem-like cell maintenance. Dysfunctional T lymphocytes—especially the accumulation of regulatory T cells—further attenuate anti-tumor immunity. Natural killer (NK) cells, dendritic cells, neutrophils, and myeloid-derived suppressor cells (MDSCs) also contribute to immune suppression through distinct yet interconnected mechanisms. Despite the success of immunotherapies in other malignancies, immune checkpoint inhibitors, CAR-T cells, and tumor vaccines have yielded limited efficacy in GBM, hindered by low neoantigen burden, antigenic heterogeneity, and poor immune infiltration. Overcoming these challenges requires a systems-level understanding of the immunoregulatory circuits within the GBM TME and the development of combination immunotherapies guided by predictive biomarkers. This review systematically delineates the roles of immune components in GBM immunopathology and outlines the emerging therapeutic strategies.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 4","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148357960","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-07-01DOI: 10.1002/biof.70130
Zhigui Chen, ShouQiang Wang, Zhou Sun, Hengyi Liao, Yue Longji, Qiang Zhang, Jie Wang
{"title":"An AI-Driven Multi-Omics Framework Identifies CASP8 as a Clinically Actionable Pyroptosis Biomarker in Bladder Cancer","authors":"Zhigui Chen, ShouQiang Wang, Zhou Sun, Hengyi Liao, Yue Longji, Qiang Zhang, Jie Wang","doi":"10.1002/biof.70130","DOIUrl":"10.1002/biof.70130","url":null,"abstract":"<div>\u0000 \u0000 <p>Despite rapid advances in multi-omics technologies, translating candidate biomarkers into clinical practice for bladder cancer remains challenging due to the difficulty of linking complex genomic instability to interpretable biological processes. To address this, we developed an AI-driven multi-omics discovery framework integrating single-cell RNA sequencing, multi-cohort transcriptomics, and machine learning–based genomic inference. By analyzing chromosomal aneuploidy and copy number variations at single-cell resolution, we identified malignant cell populations and constructed a consensus pyroptosis scoring system, followed by machine learning–assisted biomarker screening and experimental validation. Our results reveal that while global pyroptosis activity is elevated in the bladder cancer microenvironment, malignant cells with high genomic instability exhibit significant pyroptosis suppression. Through this pipeline, CASP8 was identified as a key clinically relevant biomarker; its low expression correlates strongly with increased tumor mutation burden, frequent driver gene alterations (including TP53 and RB1), and poor survival outcomes. Functional assays further confirmed that CASP8 loss promotes malignant phenotypes and alters cell death programs. Ultimately, this study establishes a next-generation framework for biomarker translation, highlighting CASP8 as a clinically actionable link between genomic instability and pyroptosis dysregulation, and demonstrating the power of AI-integrated strategies in accelerating bladder cancer research from bench to bedside.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 4","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148366730","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-06-24DOI: 10.1002/biof.70123
Yi Wu, Wanjia Chen, Siqi Gong, Jiajia Wang, Zhimin Zhai
{"title":"Platelet-Related Gene Signature Predicts Prognosis, Immune Landscape, and Drug Sensitivity in Acute Myeloid Leukemia","authors":"Yi Wu, Wanjia Chen, Siqi Gong, Jiajia Wang, Zhimin Zhai","doi":"10.1002/biof.70123","DOIUrl":"10.1002/biof.70123","url":null,"abstract":"<div>\u0000 \u0000 <p>Acute myeloid leukemia (AML) remains challenging to treat due to clinical heterogeneity and a lack of prognostic biomarkers. To address this, we developed a prognostic signature based on platelet-related genes (PRGs). By analyzing transcriptomic data from TCGA-LAML, GSE146173, and Beat AML 2.0 cohorts, we identified and validated an 11-gene signature (PSME2, PPIF, SYTL4, S100A4, CCND3, SMIM15, PARVB, STXBP5, KCNMB1, GABRE, SLC50A1) using LASSO-Cox regression. This model effectively stratified patients into high- and low-risk groups with distinct survival outcomes (<i>p</i> < 0.001) and demonstrated high predictive accuracy (1-/3-/5-year AUC: 0.832/0.782/0.880). High-risk patients exhibited immunosuppressive features, including upregulated immune checkpoints (CD274, CTLA4, HAVCR2, LAG3, PDCD1LG2, PDCD1), prominent monocyte infiltration, and reduced dendritic`11 cell activity. Drug sensitivity analysis suggested gefitinib, zebularine, and simvastatin as potential therapies for high-risk AML (<i>p</i> < 0.05). We further validated the signature's prognostic value using qPCR and clinical grouping. Notably, in vitro studies indicated that KCNMB1 facilitates AML progression. In conclusion, our robust PRG-based model elucidates the link between platelet biology, immune dysregulation, and therapeutic vulnerability in AML, offering clinical utility for risk stratification and treatment decisions.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148306792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-06-21DOI: 10.1002/biof.70128
Peter Riber Johnsen, Cecilia Pinna, Luca Andersen, Maria Vestergaard Christensen, Andrea Pinto, Sabrina Dallavalle, Hanne Ingmer, Hanne Frøkiær
{"title":"Resveratrol-Derived Dimers With Antimicrobial and Immune-Enhancing Activities","authors":"Peter Riber Johnsen, Cecilia Pinna, Luca Andersen, Maria Vestergaard Christensen, Andrea Pinto, Sabrina Dallavalle, Hanne Ingmer, Hanne Frøkiær","doi":"10.1002/biof.70128","DOIUrl":"10.1002/biof.70128","url":null,"abstract":"<p>In search for novel antibiotic candidates, polyphenols represent an unexploited source with a nearly inexhaustible number of promising compounds. In addition to the antimicrobial activity, some polyphenols modulate the immune response in a way that could enhance the clearance of invading pathogens. This study investigated four resveratrol-derived dimeric compounds, dehydro-δ-viniferin, (±)-<i>trans</i>-δ-viniferin, viniferifuran, and (±)-ε-viniferin, for their antimicrobial activity against methicillin-resistant <i>S. aureus.</i> In addition, their immunomodulating properties in bacterially challenged dendritic cells were assessed. We identified dehydro-δ-viniferin as exhibiting the most potent antimicrobial activity against methicillin-resistant <i>Staphylococcus aureus</i> with a minimal inhibitory concentration of 2 μg/mL and a minimal bactericidal concentration of 8 μg/mL, respectively. Furthermore, dehydro-δ-viniferin showed significant enhancement of the <i>S. aureus</i>-induced IL-12 production from bone marrow-derived dendritic cells, which could be ascribed to a decrease in the production of IL-10. Only if dehydro-δ-viniferin was administered to dendritic cells prior to bacterial stimulation, IL-12 production was increased; if added later, the increase in IL-12 was lost although the IL-10 production was reduced. This suggests that dehydro-δ-viniferin interferes with the signaling pathway leading to IL-10, which in turn influences the IL-12 production in a time dependent manner. Collectively, dehydro-δ-viniferin is a potent antimicrobial against methicillin-resistant <i>S. aureus</i> with enhancing effects on the bacterially induced IL-12 response in antigen-presenting cells. We therefore suggest dehydro-δ-viniferin as a promising antibiotic candidate against multidrug-resistant Gram-positive bacteria.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70128","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148293365","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":"Lysine Lactylation: Dynamic Regulation in the Tumor Microenvironment and Clinical Translational Prospects","authors":"Yimao Wu, Xiaoyan Chen, Zichang Chen, Ruowei Sun, Qian Zhang, Gokhan Zengin, Meng-Yao Li","doi":"10.1002/biof.70126","DOIUrl":"10.1002/biof.70126","url":null,"abstract":"<div>\u0000 \u0000 <p>This review systematically explores the dynamic regulatory roles of lysine lactylation (Kla) in the tumor microenvironment (TME) and its clinical translational potential. As an emerging post-translational modification, Kla modifies histones and non-histone proteins via lactate generated by the Warburg effect, thereby reshaping tumor metabolism and immune landscapes. Mechanistically, Kla orchestrates metabolic reprogramming and immunosuppression through key signaling pathways such as HIF-1α, mTOR, and NF-κB. Specifically, it promotes the activation of immunosuppressive cells while inhibiting cytotoxic CD8<sup>+</sup> T cells and NK cells, fostering tumor immune escape. Preclinical studies demonstrate that targeting lactate metabolism or lactylation enzymes restores immune effector functions and enhances immune checkpoint therapy efficacy. However, challenges such as tumor heterogeneity, metabolic plasticity, and systemic toxicity remain. Future research should focus on Kla's crosstalk with other epigenetic modifications, spatiotemporal dynamics in TIME, and clinical translation to unlock its potential as a biomarker and precision oncology target.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.2,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148275570","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-06-13DOI: 10.1002/biof.70124
Abhishek Kumar, Debasish Kumar Ghosh
{"title":"Lipid Codes and Lipid-Binding Proteins as Central Regulators of Autophagy","authors":"Abhishek Kumar, Debasish Kumar Ghosh","doi":"10.1002/biof.70124","DOIUrl":"https://doi.org/10.1002/biof.70124","url":null,"abstract":"<div>\u0000 \u0000 <p>Autophagy is increasingly understood as a lipid-governed membrane program rather than a solely protein-driven degradative pathway. This review combines molecular and mechanistic evidence showing how lipid molecules, metabolic enzymes, and membrane physical properties coordinate autophagy from induction to lysosomal degradation. We highlight phosphoinositide microdomains and their cognate kinases and phosphatases as spatial cues that nucleate phagophores, control maturation, and regulate lysosome reformation. We also discuss alternative phosphoinositide sources, sphingolipid and ceramide signaling, phosphatidic acid and diacylglycerol metabolism, fatty-acyl composition, and acyl-CoA signaling as determinants of membrane curvature, tension, leaflet asymmetry, and phase behavior in autophagy. Key protein effectors and their lipid binding motifs and domains are integrated into a model in which lipid chemistry and mechanics gate enzymatic activities. We present integrated lipid-protein-biophysics approaches to highlight outstanding questions and uncover predictive principles.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148238173","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-06-01DOI: 10.1002/biof.70120
Chengyu Zang, Ran Zhao, Zhang Feng, Linfeng Zhang, Chunyan Liu, Siyuan Yin, Ru Song, Zhenjie Wu, Linqi Su, Yibing Wang
{"title":"Mesenchymal Stem Cell-Derived Exosomal miR-29a-3p Improves Hypertrophic Scar by Inhibiting the Proliferation and Migration of Schwann Cells via the PDGFRB/PAK1 Axis","authors":"Chengyu Zang, Ran Zhao, Zhang Feng, Linfeng Zhang, Chunyan Liu, Siyuan Yin, Ru Song, Zhenjie Wu, Linqi Su, Yibing Wang","doi":"10.1002/biof.70120","DOIUrl":"10.1002/biof.70120","url":null,"abstract":"<div>\u0000 \u0000 <p>Mesenchymal stem cell-derived exosomes (MSC-exo) can alleviate hypertrophic scar (HS) formation, whereas Schwann cells (SCs) promote HS formation. This study aimed to investigate whether MSC-exos attenuate HS by modulating SCs and to elucidate the underlying mechanisms. HS and normal skin tissues were obtained from patients. MSCs, SCs, and fibroblasts were isolated from BALB/c mice. SCs and HS mouse models were treated with MSC-exos. SCs under various treatments were co-cultured with fibroblasts. mRNA and protein levels were assessed by qRT-PCR, western blot, immunofluorescence, and immunohistochemical staining. Cell migration, proliferation, and apoptosis were evaluated by wound healing assay, CCK-8 assay, and TUNEL assay, respectively. HS tissue morphology was examined by Hematoxylin–eosin and Masson staining. The targeting of miR-29a-3p towards PDGFRB was validated using a dual-luciferase reporter assay. In patient HS tissues, downregulated miR-29a-3p was negatively correlated with upregulated PDGFRB. MSC-exo-delivered miR-29a-3p suppressed SCs proliferation and migration, promoted SCs apoptosis, and reduced SCs-secreted NGF, thereby inhibiting fibroblast migration and myofibroblast transformation. These effects were reversed by miR-29a-3p knockdown in MSCs. Furthermore, miR-29a-3p targeted and inhibited PDGFRB expression in SCs. Silencing PDGFRB abolished the promoting effects of miR-29a-3p inhibition on SCs, which was rescued by the PAK1 activator FTY720. MSC-exo-delivered miR-29a-3p ameliorates HS by inhibiting SCs proliferation, migration and NGF secretion via the PDGFRB/PAK1 axis to suppress myofibroblast transformation. Beyond the traditional focus on fibroblasts, this reveals an exosome-SCs-fibroblast network, providing a novel theoretical basis for HS treatment.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148142596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-05-31DOI: 10.1002/biof.70121
Qun Zeng, Shitian Huang, Tingting Jiang
{"title":"The Multiple Roles and Targeting Strategies of LonP1 in the Occurrence and Development of Cancer","authors":"Qun Zeng, Shitian Huang, Tingting Jiang","doi":"10.1002/biof.70121","DOIUrl":"10.1002/biof.70121","url":null,"abstract":"<div>\u0000 \u0000 <p>LonP1, a mitochondrial AAA+ protease, serves as a pivotal integrator of mitochondrial quality control (MQC) and metabolic reprogramming in cancer progression. Alternative splicing generates three functionally distinct isoforms: full-length ISO1 maintains mitochondrial homeostasis by degrading oxidized proteins and stabilizing mitochondrial transcription factor A (TFAM) for mtDNA integrity; truncated ISO2 (Δ42–105 AA) drives glycolytic reprogramming and epithelial-mesenchymal transition (EMT) by upregulating Snail/vimentin; and cytoplasmic ISO3 (Δ1–196 AA) lacks protease activity and is tumor-irrelevant. Tumor microenvironment (TME) cues (hypoxia, <i>H. pylori</i> infection, PFOA exposure, glutamine depletion) regulate LonP1 via Akt phosphorylation/Sirt3 deacetylation, coordinating MQC and metabolic adaptation to support cancer cell survival and metastasis. Functional data confirm its pro-tumor role: LonP1 upregulation enhances cervical cancer mitophagy and gastric cancer glycolysis, while knockdown induces mitochondrial dysfunction and apoptosis. This review summarizes current advances by (1) systematically integrating the isoform-specific functions of LonP1; (2) constructing a “LonP1-MQC-metabolism” regulatory network based on published evidence; and (3) proposing isoform-specific targeted strategies for precision oncology. These insights position LonP1 as a promising candidate for precision oncology, offering a cohesive understanding of mitochondrial regulation in cancer.</p>\u0000 </div>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BioFactorsPub Date : 2026-05-31DOI: 10.1002/biof.70059
{"title":"Correction to “SUMO-Specific Proteases: SENPs in Oxidative Stress-Related Signaling and Diseases”","authors":"","doi":"10.1002/biof.70059","DOIUrl":"10.1002/biof.70059","url":null,"abstract":"<p>Jiao, Y. Zhang, X. Yang, Z “SUMO-specific proteases: SENPs in oxidative stress-related signaling and diseases”, BioFactors. 2024; 50: 910-921.</p><p>The listed affiliation Division of Oncology, Department of Clinical and Medical Sciences, Lund University for the author Yang Z was incorrect. Lund University has stated the research in the article was not associated in any way with the university. The affiliation has been removed and replaced with South China Agricultural University.</p><p>We apologize for this error.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":"52 3","pages":""},"PeriodicalIF":5.0,"publicationDate":"2026-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.70059","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136324","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}