Journal of Cellular Physiology最新文献

{"title":"RETRACTION: Notch Activation Promotes Osteoblast Mineralization by Inhibition of Apoptosis.","authors":"","doi":"10.1002/jcp.70191","DOIUrl":"https://doi.org/10.1002/jcp.70191","url":null,"abstract":"<p><strong>Retraction: </strong>Y. Xu, B. Shu, Y. Tian, M. Chelly, M.M. Morandi, S. Barton, X. Shang, and Y. Dong, \"Notch Activation Promotes Osteoblast Mineralization by Inhibition of Apoptosis,\" Journal of Cellular Physiology 233, no. 10 (2018): 6921-6928, https://doi.org/10.1002/jcp.26592. The above article, published online on April 25, 2018, in Wiley Online Library (http://onlinelibrary.wiley.com/), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath, and Wiley Periodicals LLC. Concerns were raised to the journal editorial office, as well as on PubPeer [1], regarding multiple duplicated images in the figures. Following investigation, evidence of duplication was found within Figure 2A; between Figure 2A of this article and Figure 2B of a different article by some of the same authors [Shu et al. 2017: https://doi.org/10.1038/s41598-017-07633-7]; and between Figure 4A of this article and Figure 3 of a different article by some of the same authors [Tian et al. 2017: https://doi.org/10.1038/cddis.2017.2]. The authors cooperated with the investigation and sent a proposed correction, but this was not considered sufficient to resolve the concerns. The editor has lost confidence in the results reported, and therefore, the article must be retracted. The authors disagree with the decision. Reference: [1] B. Tianmuensis, \"Notch Activation Promotes Osteoblast Mineralization by Inhibition of Apoptosis,\" PubPeer, 2025, https://pubpeer.com/publications/0AC64BDE43F94128FC9819A85657DF.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70191"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modeling and Characterization of Intestinal Senescence Using Human Organoids: Insights Into the Epithelial to Mesenchymal Transition.","authors":"Tatsuhiro Ayabe, Yu Takahashi, I-Ting Lee, Takeshi Kokubo, Yoshio Yamauchi, Ryuichiro Sato","doi":"10.1002/jcp.70181","DOIUrl":"10.1002/jcp.70181","url":null,"abstract":"<p><p>Intestinal senescence is an important factor in systemic aging and age-related diseases; however, detailed studies have been limited due to the lack of robust experimental models. In this study, we established cellular senescence models of human small intestinal organoids using two senescence-inducing agents: butyrate (an endogenous microbial metabolite) and cisplatin (an exogenous chemotherapeutic agent). Both molecules induced senescence-associated features, including increased p16INK4a, CDKN1A, IL8, and TNF expression, as well as SA-β-Gal activity. RNA-sequencing revealed that cisplatin, but not butyrate, activated the p53 signaling pathway, whereas both downregulated various nutrient absorption and metabolism-related pathways. These models exhibited reduced nutrient transporter expression, diminished glucose uptake, and decreased vitamin D responsiveness, thus recapitulating the features of aged or damaged intestinal tissue. In cisplatin-treated organoids, epithelial to mesenchymal transition (EMT)-related gene ontologies were enriched based on RNA-sequencing. The induction of EMT through cisplatin-induced senescence was further confirmed by EMT marker gene expression, which decreased following the inhibition of TGF-β signaling, a canonical EMT-inducing pathway. Notably, TGF-β signaling inhibition attenuated senescence-induced inflammation and nutrient dysfunction, which suggests the importance of EMT as a target for preventing intestinal senescence. Our models provide a novel platform for examining the intestine-specific molecular mechanisms of senescence associated with distinct senescence-inducing mechanisms and for developing strategies to prevent age-related intestinal dysfunction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70181"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148030969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding the Hexosamine Biosynthesis Pathway: Implications for Novel Therapeutic Strategies in Sarcoma.","authors":"Pegah Rahimizadeh, Richard Miallot, Chelsea De Bellis, Philippe Jolivet, Joanna Przybyl","doi":"10.1002/jcp.70182","DOIUrl":"10.1002/jcp.70182","url":null,"abstract":"<p><p>Cancer cells rewire their metabolism to sustain a high proliferation rate. Sensing external cues is essential to match the metabolic fluxes of the cells to the external stimuli. As part of the glucose metabolism, the hexosamine biosynthesis pathway (HBP) is considered a nutrient-sensing pathway. The HBP produces UDP-GlcNAc, a key precursor for N-linked glycosylation, O-linked glycosylation, and O-GlcNAcylation. These post-translational modifications can influence protein folding, interactions, and subcellular localization. Altered glycosylation of oncogenic proteins has been linked to the acquisition of malignant properties. In this review, we outline the current knowledge of molecular alterations and the prognostic role of the expression of HBP enzymes in sarcoma. We catalog the known sites of N-/O-linked glycosylation and O-GlcNAc modifications in molecular drivers of mesenchymal tumors, and discuss the potential effect of these modifications on protein function. We also summarize the studies that examined the effect of the HBP inhibitors in preclinical models of cancer, and explore the potential of the HBP inhibition as a novel therapeutic approach for sarcoma. Finally, we present recent progress in drug development for targeting the HBP, and delineate the key technological innovations needed to accelerate the preclinical and clinical research on pharmacological inhibition of the HBP.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70182"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13159415/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Scaffold Protein PDLIM5 Regulates TRPC1 Calcium Channel Mediated Store-Operated Calcium Entry in Mouse Myoblasts.","authors":"Mingyi Dong, Tomoaki Niimi, Andrés Daniel Maturana","doi":"10.1002/jcp.70173","DOIUrl":"10.1002/jcp.70173","url":null,"abstract":"<p><p>Intracellular calcium (Ca²⁺) signaling controls myoblast proliferation, fusion, and myofiber formation. In myoblasts, Transient Receptor Potential Canonical (TRPC) channels, with TRPC1 as a predominant isoform, mediate store-operated Ca²⁺ entry (SOCE) and are essential for myogenesis. PDLIM5 (ENH1), a PDZ-LIM scaffold protein, organizes signaling events, including ion channel regulation and transcriptional control in muscles. This study aims to test the hypothesis that PDLIM5 regulates TRPC1-mediated Ca²⁺ entry in myoblasts. Thapsigargin-induced SOCE was suppressed by the SOCE inhibitors Gd³⁺ and 2-APB, as well as by TRPC1 siRNA, supporting the involvement of TRPC1 in SOCE in C2C12 myoblasts. Additionally, SOCE inhibition decreased the number of nuclei per myotube and reduced the size of myotubes. ENH1 siRNA knockdown significantly downregulated TRPC1 and STIM1 mRNA expression, increased basal cytosolic Ca²⁺ level, and impaired SOCE response and myotube maturation. Overexpression of ENH4, a skeletal muscle-specific short splice variant of ENH1, similarly repressed TRPC1-mediated SOCE and myotube formation. Conversely, ENH1 overexpression enhanced SOCE without altering the mRNA levels of TRPC1, Orai1, or STIM1. Immunoprecipitation showed a physical interaction between ENH1/ENH4 and TRPC1. In differentiated myotubes, TRPC1 also contributed to thapsigargin-induced SOCE, as evidenced by the reduced Ca²⁺ entry following TRPC1 knockdown. ENH1 knockdown and ENH4 overexpression significantly attenuated SOCE in myotubes; notably, ENH1 knockdown also increased basal cytosolic Ca²⁺ level. In contrast to myoblasts, ENH1 overexpression did not enhance SOCE in myotubes, concomitant with the absence of a detectable interaction between ENH1 and TRPC1, whereas ENH4 retained its association with TRPC1. These findings suggest that ENH1 and ENH4 differentially modulate TRPC1-dependent Ca²⁺ entry in C2C12 cells, thereby regulating myogenic differentiation and contributing to skeletal muscle formation and development.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70173"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838525","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum- and Glucocorticoid-Regulated Kinase 1 Regulates Spindle Assembly Through RanBP1 During Oocyte Meiosis.","authors":"Li-Shu Li, Shu-Jie Yang, Xiao-Qing Li, Xing Duan","doi":"10.1002/jcp.70196","DOIUrl":"10.1002/jcp.70196","url":null,"abstract":"<p><p>Advanced maternal age is associated with increased oocyte aneuploidy and early miscarriage. Serum- and glucocorticoid-regulated kinase 1 (SGK1), a member of the serine/threonine kinase family, is downregulated in oocytes from aged mice. However, the mechanisms by which SGK1 controls oocyte maturation remain unclear. Here, we show that SGK1 localizes predominantly to spindle poles during oocyte maturation. Knockdown of SGK1 via siRNA or pharmacological inhibition disrupts spindle assembly and impairs kinetochore-microtubule attachments in mouse oocytes. This disruption leads to sustained activation of the spindle assembly checkpoint, failure of Cyclin B1 and Securin degradation, impaired metaphase I-anaphase transition, and defective first polar body extrusion. Mechanistically, we identify RanBP1 as a potential mediator of SGK1 function during meiotic progression. In porcine oocytes, SGK1 inhibition similarly compromises maturation and Cyclin B1 degradation, suggesting a conserved role across mammalian species. Together, our findings establish SGK1 as a critical regulator of spindle assembly and meiotic progression in mammalian oocytes.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70196"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042436","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Role of Epithelial-Mesenchymal Transition in Oral Inflammatory Diseases.","authors":"Yuyi Wang, Yi Yang, Chunmei Xu, Peilei Shi, Jun Wang, Yi Ding, Xudong Xie","doi":"10.1002/jcp.70194","DOIUrl":"10.1002/jcp.70194","url":null,"abstract":"<p><p>Epithelial-mesenchymal transition (EMT) refers to a process in which epithelial cells shed their polarity and intercellular adhesion while adopting mesenchymal traits. Emerging evidence indicates that EMT is critically involved in the pathogenesis of several oral inflammatory diseases, including periodontitis, drug-induced gingival overgrowth, and Sjögren's syndrome. A thorough understanding of the molecular mechanisms governing EMT may help elucidate the pathogenesis of these diseases and provide new diagnostic and therapeutic strategies for clinical practice. This review will focus on the recent research progress regarding the role of EMT in the above three oral inflammatory diseases, with the aim of offering insights for related research and clinical applications.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70194"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148042458","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell Membrane Biogenesis: A Matter of Survival. Its Role in Renal Epithelia Restitution After Calcium Oxalate Injury.","authors":"Leandro Gaston Parra, Dylan Ezequiel Sendyk, Sandra Viviana Verstraeten, Ailén Florencia Salafia, Nicolás Octavio Favale, Emanuel Morel Gómez, María Del Carmen Fernández Tome, Cecilia Irene Casali","doi":"10.1002/jcp.70187","DOIUrl":"10.1002/jcp.70187","url":null,"abstract":"<p><p>Calcium oxalate (CaOx) is the main component of kidney stones. These stones interact with the surface of renal epithelial cells and initiate injury. In differentiated renal epithelial cells (DREC), we demonstrated that oxalate (Oxa) injures monolayers, which undergo a type II epithelial-mesenchymal transition during the first 24 h (the damage period). Thereafter, cells gradually recover their morphology, restituting the monolayer between 48 and 72 h (the restitution period). Since Oxa induces lipid peroxidation (LPO), which disrupts membrane homeostasis, we hypothesize that epithelial restitution occurs after the activation of lipid metabolism and the restoration of cellular membrane integrity. The goal of this study was to determine the role of glycerolipid (GL) metabolism in DREC monolayer survival and restitution after Oxa injury. DREC monolayers were incubated with 1.5 mM Oxa during the damage and the restitution periods. After the damage period, we found alterations in the DREC monolayer and a decrease in cell number. Moreover, Oxa-induced LPO changes membrane composition and properties. These changes were accompanied by the activation of glycerophospholipid (GP) and triacylglyceride (TG) synthesis and by an increase in the number of lipid droplets (LD), but a decrease in their size. The inhibition of lipin activity impaired GP and TG synthesis, completely preventing DREC monolayer restitution. Collectively, these results demonstrate that Oxa-induced LPO disrupts DREC membrane properties, changing their biophysics and composition, which affects cell physiology. To restore cell homeostasis, GL synthesis and LD biogenesis are activated, allowing the gradual recovery of the DREC monolayer phenotype, and highlighting the importance of membrane structure maintenance in cell survival.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70187"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838366","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Mechanisms of Programmed Cell Death Pathways in Chronic Obstructive Pulmonary Disease.","authors":"Yuchen Zhuang, Lan Yao, Wenchuan Qi","doi":"10.1002/jcp.70177","DOIUrl":"10.1002/jcp.70177","url":null,"abstract":"<p><p>Chronic obstructive pulmonary disease (COPD) represents a prevalent respiratory ailment, which is distinguished by enduring airflow obstruction and a tendency to progress over time. Over 400 million people globally are currently impacted. Alveolar epithelial cells, airway epithelial cells, and important inflammatory cell populations are all actively involved in the pathological development of COPD. These cells' interactions have wide-ranging physiological effects on the body, such as aggravating lung damage and inducing inflammation, which are the pathogenic causes of COPD. In the present review, numerous programmed cell death (PCD) modes are addressed with a focus on molecular mechanisms and crosstalk of seven PCD processes-apoptosis, necroptosis, ferroptosis, autophagy, pyroptosis, cuproptosis, and disulfidptosis-in COPD pathogenesis and initiation. It also refers to clinical treatment strategies for the acute and stable phases of COPD based on PCD regulation. From the cellular perspective, we may have a more exact understanding of disease phenotypes; demystification of cell-type-specific mechanisms is aimed at providing theoretical guidance for further probing of COPD's molecular pathology and development of novel therapeutic strategies against PCD.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70177"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147815412","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Probiotic Combination of Limosilactobacillus reuteri and Clostridium butyricum Ameliorates 5-Fluorouracil-Induced Intestinal Mucositis in Rats by Strengthening Barrier Integrity and Modulating Immuno-Microbial Homeostasis.","authors":"Pui-Ying Leong, Wen-Chen Chuang, Jiunn-Liang Ko, Jiunn-Wang Liao, Liang-Chuan Chen, Yi-Hsuan Tsai, Chu-Chyn Ou","doi":"10.1002/jcp.70183","DOIUrl":"10.1002/jcp.70183","url":null,"abstract":"<p><p>5-fluorouracil (5FU)-induced intestinal mucositis significantly limits its clinical utility and compromises patient outcomes. Building on our previous finding that a specific probiotic formulation, consisting of Limosilactobacillus reuteri BCRC 80379 and Clostridium butyricum MIYAIRI 588 (collectively referred to as LCs), mitigated cisplatin-induced mucositis, this study evaluated the prophylactic efficacy and underlying mechanisms of LCs against 5FU-induced mucositis in Wistar rats. Rats were divided into control, 5FU-only, and 5FU+LCs groups. LCs was orally administered daily for 21 days before and throughout the 5FU treatment (50 mg/kg/day for 5 days). Intestinal tissues were analyzed using histological, molecular, and microbiological approaches. Pretreatment with LCs significantly attenuated 5FU-induced small intestinal damage, as evidenced by improved mucosal structure (e.g., increased villus height, crypt depth, and goblet cell density), along with reduced inflammatory cell infiltration. Moreover, LCs reinforced the intestinal barrier by upregulating genes associated with the mucus layer (Muc2) and tight junctions (Ocln, Tjp1, and Cldn1). LCs also suppressed the TLR4/MyD88/NF-κB pathway, leading to reduced levels of pro-inflammatory mediators (e.g., TNF-α, IL-1β, and MPO) while elevating key regulatory mediators such as IL-10 and secretory IgA (sIgA). Furthermore, microbial profiling revealed that LCs beneficially reshaped gut microbiota composition by reducing opportunistic pathogens (e.g., Escherichia-Shigella and Enterobacter). These microbial changes were accompanied by a favorable immune modulation, including decreased pro-inflammatory markers and increased homeostatic mediators. Collectively, these findings suggest that LCs mitigates 5FU-induced mucositis through coordinated regulation of intestinal barrier integrity, immune responses, and gut microbiota, highlighting its potential as a probiotic-based approach for managing chemotherapy-induced intestinal injury.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70183"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147972881","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Progranulin and Inflammation-Induced Cancer: An Important Player in the Tumor Microenvironment?","authors":"Gaia Insinga, Caterina Tomassetti, Vrunda Satasiya, Francesca Gimigliano, Antonio Giordano, Emanuele Giurisato, Andrea Morrione","doi":"10.1002/jcp.70188","DOIUrl":"10.1002/jcp.70188","url":null,"abstract":"<p><p>Progranulin (PGRN) is a multifunctional glycoprotein recognized as a key regulator at the intersection of tumor progression and inflammation. Originally described as a mitogenicgrowth factor within the tumor. PGRN is now known to exert a broad spectrum of biological effects within the tumor microenvironment (TME), where it functions as both an oncogenic driver and an immunomodulatory molecule. Beyond its capacity to promote tumor cell proliferation, migration, and epithelial-mesenchymal transition (EMT). PGRN critically shapes the inflammatory and stromal landscape that sustains tumor growth. This review aims to comprehensively summarize current knowledge on the multifaceted roles of PGRN within the TME, with a particular focus on its functions in immune and stromal cells that contribute to tumor progression and immune evasion. In fact, it reprograms TME toward an immunosuppressive state by activating signaling pathways such as TNFR2/STAT3 and PI3K/AKT. It promotes M2-like macrophage polarization, enhances PD-L1 expression, supports regulatory T-cell stability, and suppresses CD8⁺ T- and NK-cell cytotoxicity, and fosters immune evasion. Simultaneously, PGRN affects stromal components by activating cancer-associated fibroblasts (CAFs), remodeling the extracellular matrix, and stimulating angiogenesis. These coordinated actions position PGRN as a central orchestrator of tumor-associated inflammation. Despite these insights, its roles in myeloid-derived suppressor cells, neutrophils, and other stromal subsets remain poorly understood. Therefore, investigating PGRN's influence on these cells is crucial for understanding tumor progression and therapeutic resistance and may reveal novel strategies to disrupt PGRN-dependent inflammatory circuits and enhance anti-tumor immunity.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70188"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147868593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}