Journal of Cellular Physiology最新文献

{"title":"Mast Cell Immunometabolism in Type 2 Diabetes and Alzheimer's Disease","authors":"Heather L. Caslin,&nbsp;Munira Kapadia,&nbsp;Tameka A. Clemons","doi":"10.1002/jcp.70091","DOIUrl":"https://doi.org/10.1002/jcp.70091","url":null,"abstract":"<div>\u0000 \u0000 <p>Type 2 diabetes (T2D) and Alzheimer's Disease (AD) have seemingly different pathologies and symptoms. However, T2D is a risk factor for AD, and recent evidence suggests there are many mechanistic similarities between the etiologies of each disease including inflammation. Mast cells are tissue resident, sentinel immune cells that reside in the pancreas, adipose tissue, and brain, increase in T2D and AD, and have generally been shown to worsen T2D and AD. However, there are limited studies of local or temporal mast cell deletion, and different phenotypic and polarization states seemingly influence the role of mast cells in the progression of disease. As there are metabolic similarities between T2D and AD including insulin resistance and lipid influx into the brain, we discuss the impact of glucose, insulin, amylin, and different lipid species on the activation and polarization of mast cells, which generally reduce IgE-mediated degranulation and promote lipid droplet formation and arachidonic acid metabolism. Altogether, this review provides a framework for understanding a shared mechanism of immunometabolic regulation of T2D and AD and provides rationale for future work in this area.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145062496","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 Age-Associated Long Noncoding RNA lnc81 Regulates Ovarian Granulosa Cell Proliferation and Apoptosis Through TEAD2-CCN1/2 Pathway in Mice","authors":"Zhangqiang Ma,&nbsp;Ruichen Luo,&nbsp;Yue Xue,&nbsp;Liping Zheng,&nbsp;Chong Zhou,&nbsp;Sitian Fang,&nbsp;Na Hu,&nbsp;Houpeng Wang,&nbsp;Xiu Cheng,&nbsp;Tao Luo,&nbsp;Liaoliao Hu","doi":"10.1002/jcp.70090","DOIUrl":"https://doi.org/10.1002/jcp.70090","url":null,"abstract":"<div>\u0000 \u0000 <p>Ovarian granulosa cells (GCs) are pivotal for follicular homeostasis, and their dysregulated apoptosis drives age-related ovarian aging. The Hippo signaling pathway, modulated by long noncoding RNAs (lncRNAs), is implicated in regulating GCs proliferation and ovarian aging. TEAD2 (Transcriptional Enhanced Associate Domain 2), a key downstream transcription factor of the Hippo signaling pathway, plays a critical role in regulating cell proliferation, apoptosis, and embryonic stem cell self-renewal. However, the precise molecular mechanisms by which lncRNAs influence the Hippo pathway in GCs are not fully understood. Through comprehensive RNA-seq analysis of ovarian tissues across three distinct age groups (3-, 11-, and 17-month-old mice), we identified lnc81 as a senescence-associated lncRNA that physically interacts with TEAD2. RNA immunoprecipitation (RIP) assays demonstrated direct binding between lnc81 and TEAD2, while subcellular fractionation coupled with qRT-PCR revealed predominant nuclear localization of lnc81 in granulosa cells (GCs). Importantly, lnc81 expression exhibited a progressive, age-dependent elevation during ovarian aging. Functional characterization showed that lnc81 knockdown in GCs significantly: (i) Inhibited cellular proliferation (as evidenced by decreased <i>Pcna</i> expression). (ii) Promoted apoptosis (indicated by increased BAX/BCL-2 ratio and elevated TUNEL-positive cells). Mechanistically, while lnc81 depletion upregulated CCN1/CCN2 protein levels, it did not affect TEAD2 expression, suggesting that lnc81 regulates TEAD2 transcriptional activity rather than modulating its protein stability. Our findings highlight lnc81 as a nuclear lncRNA that interacts with TEAD2 to amplify CCN1/CCN2 signaling, thereby promoting GC apoptosis and ovarian aging. This mechanistic insight positions lnc81 as a potential biomarker for age-related ovarian decline and a candidate target for therapeutic intervention.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145022296","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":"RETRACTION: Novel Oral Transforming Growth Factor-β Signaling Inhibitor Potently Inhibits Postsurgical Adhesion Band Formation","authors":"","doi":"10.1002/jcp.70089","DOIUrl":"https://doi.org/10.1002/jcp.70089","url":null,"abstract":"<p><b>RETRACTION:</b> A. Soleimani, F. Asgharzadeh, F. Rahmani, et al. “Novel Oral Transforming Growth Factor-β Signaling Inhibitor Potently Inhibits Postsurgical Adhesion Band Formation.” <i>Journal of Cellular Physiology</i> 235, no. 5 (2019): 1349-1357, https://doi.org/10.1002/jcp.29053.</p><p>The above article, published online on 17 July 2019 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by the third party, which revealed multiple inconsistencies found in Figure 2(g) and Figure 4(a), and additional inconsistencies were found in Figure 1(d). The explanation and raw data provided by the authors could not sufficiently address these concerns. Overall, the editors have lost confidence in the integrity and reliability of the full body of data presented in the article and consider the conclusions of this manuscript substantially compromised. The authors disagree with the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70089","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145011932","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":"Single-Cell Sequencing-Based Exploration of the Role of Tip Cells on Astrocytes and Macrophages After Spinal Cord Injury","authors":"Xiaolin Zeng,&nbsp;Yuni Long,&nbsp;Gang Li,&nbsp;Di Zhang,&nbsp;Yilong Deng,&nbsp;Xin Zhi,&nbsp;Yong Wan,&nbsp;Le Wang,&nbsp;Xiang Li","doi":"10.1002/jcp.70088","DOIUrl":"https://doi.org/10.1002/jcp.70088","url":null,"abstract":"<div>\u0000 \u0000 <p>Excessive inflammation is a capital cause of scar formation and inflammation microenvironment that result in challenge of axonal regeneration after spinal cord injury (SCI). Macrophages and astrocytes play important roles in the inflammatory response. Tip cells, a critical endothelial sub-population, play pivotal roles in post-injury vascular regeneration. Nevertheless, their characteristics in SCI remain poorly documented. This study based on single cell RNA sequencing (scRNA-seq) and in vitro experiment, investigates the effects of tip cells on astrocytes and macrophages. For astrocytes, tip cells can recruit astrocytes to migrant, contribute to the formation of fence-like structure of astrocytes, finally inhibit the diffusion of inflammation via the Angptl4-Sdc4 ligand-receptor pathway. For macrophages, similarly through the Angptl4-Sdc4 ligand-receptor pathway, tip cells can promote macrophages to polarize more toward the M2 phenotype and inhibit their polarization toward M1 phenotype, thus alleviate the inflammatory response. Tip cells after SCI exhibit conserved ribosomal protein expression, implicating ribosome-dependent signaling in their function. These finding highlight the critical role of tip cells in microenvironment after SCI, offering a potential treatment target for SCI.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 9","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144927670","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":"Regulation of Ghrelin Production and Food Intake by Gastric Adenylyl Cyclase Type 8","authors":"Shaohong Wu,&nbsp;Handan Deng,&nbsp;Ruili Yu,&nbsp;Quan Yu,&nbsp;Wei Li,&nbsp;Yawen Zhao,&nbsp;Ke Yang,&nbsp;Luyang Gao,&nbsp;Geyang Xu","doi":"10.1002/jcp.70087","DOIUrl":"https://doi.org/10.1002/jcp.70087","url":null,"abstract":"<div>\u0000 \u0000 <p>Ghrelin is a peptide hormone primarily produced by ghrelin cells in the stomach, playing a vital role in the regulation of eating behavior. Adenyl cyclase 8 (ADCY8), a key downstream signaling factor of G protein-coupled receptors, is essential for maintaining energy homeostasis by modulating levels of cyclic adenosine monophosphate (cAMP). Nevertheless, how ADCY8 modulates ghrelin levels and affects food intake is not well understood. Our findings demonstrated that <i>Adcy8</i>^{<i>−/−</i>} mice exhibited elevated levels of ghrelin and increased food consumption under both normal and high-fat diet conditions. These changes were associated with a reduction in the activity of the cAMP-PKA-mTOR signaling pathway within the gastric mucosa. The administration of the ghrelin receptor antagonist <span>d</span>-Lys-3-GH-releasing peptide-6 significantly decreased calorie intake in both wild-type and <i>Adcy8</i>^{<i>−/−</i>} mice. Furthermore, forskolin was shown to inhibit ghrelin and calorie intake in normal mice, an effect that was absent in <i>Adcy8</i>^{<i>−/−</i>} mice. Treatment with forskolin or overexpression of <i>Adcy8</i> in both primary ghrelin-producing cells and mHypoE-42 cells resulted in decreased ghrelin levels, accompanied by activation of the cAMP-PKA-mTOR signaling pathway. Conversely, the use of the inhibitor SQ22536 or knockdown of <i>Adcy8</i> produced opposing effects. In conclusion, gastric ADCY8 regulates the expression and secretion of ghrelin via the cAMP-PKA-mTOR signaling pathway, thereby influencing food intake.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144910192","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":"RETRACTION: Involvement of Notch-1 in Resistance to Regorafenib in Colon Cancer Cells","authors":"","doi":"10.1002/jcp.70082","DOIUrl":"https://doi.org/10.1002/jcp.70082","url":null,"abstract":"<p><b>RETRACTION:</b> G. Mirone, S. Perna, A. Shukla, G. Marfe, “Involvement of Notch-1 in Resistance to Regorafenib in Colon Cancer Cells,” <i>Journal of Cellular Physiology</i> 231, no. 5 (2015): 1097-1105, https://doi.org/10.1002/jcp.25206.</p><p>The above article, published online on 30 September 2015 in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Robert Heath; and Wiley Periodicals LLC. The retraction has been agreed due to concerns raised by the third party, which revealed inappropriate figure duplications in Figure 5B and Figure 7D, by different groups of authors in different articles. In addition, there are inconsistencies in Figure 2B. The corresponding author has responded in accordance with the concerns and provided the original western blots for Figure 5B and explanation for Figure 2B. However, data issues were found in the last authors' other articles and the Editor-in-Chief now has lost confidence in the integrity and reliability of the full body of data presented in the article and consider the conclusions of this manuscript substantially compromised. The authors were informed of the retraction.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70082","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144888203","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":"Connexin 43 Role in Mitochondrial Transfer and Homeostasis in the Central Nervous System","authors":"Anna Gervasi,&nbsp;Simona D'Aprile,&nbsp;Simona Denaro,&nbsp;Maria Angela Amorini,&nbsp;Nunzio Vicario,&nbsp;Rosalba Parenti","doi":"10.1002/jcp.70086","DOIUrl":"https://doi.org/10.1002/jcp.70086","url":null,"abstract":"<p>Connexin 43 (Cx43) is a transmembrane protein involved in the assembly of gap junctions (GJs) and hemichannels (HCs), organized structures that allow the transferring of ions and small signaling molecules between cells and/or extracellular environment, thereby contributing to tissue homeostasis intercellular communication. Cx43 has recently been identified within the mitochondria of cells, suggesting that it may have additional functions beyond its canonical role. Most studies of mitochondrial Cx43 (mt-Cx43) have been limited to cells of the cardiovascular system, where it appears to play a role in ATP production, calcium homeostasis, and the response to oxidative stress. However, its functions within the central nervous system (CNS) are not fully understood. Recently, it has been observed that Cx43-forming GJs is one of the key mechanisms that cells use for the transfer of organelles, including mitochondria. Cx43-mediated mitochondrial transfer is crucial in the CNS, supporting cellular homeostasis and neuroprotection under both physiological and pathological conditions. The dual roles of Cx43 in regulating mitochondrial function and in mediating mitochondrial transfer, raise important questions about how it coordinates these mechanisms. Herein, we reviewed recent findings on the importance of Cx43 and mt-Cx43 in the healthy and altered CNS environment, with the aim of shedding light on its potential role in CNS homeostasis and as a therapeutic target in neurological disorder in which Cx43 plays a predominant function.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/jcp.70086","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144881461","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":"View Micronuclei in the Extent of Evolution: New Insight Into an Old Issue","authors":"Shangzhi Yang,&nbsp;Haiyang Yao,&nbsp;Ying Zhang,&nbsp;Wenchuan Zhang,&nbsp;Shiqi Jin,&nbsp;Kainan Huang,&nbsp;Juan Song,&nbsp;Yan Feng,&nbsp;Xiaoguang Li,&nbsp;Xianli Wang","doi":"10.1002/jcp.70079","DOIUrl":"https://doi.org/10.1002/jcp.70079","url":null,"abstract":"<div>\u0000 \u0000 <p>Micronuclei (MNs), once regarded as cellular debris or genotoxicity markers, can also be recognized as dynamic structures with potential evolutionary significance. In tumor models, MNs promote clonal diversification, mutagenesis, and adaptation. MNs' interaction with the conserved cGAS-STING pathway reflects dual roles in immune defense for the individual and adaptive response for cell under stress. MNs may also contribute to aging-related evolution and be functional in embryonic development. MN's presence and function across species suggests the ability of MN to offer genomic diversity and selective advantage. Therefore, our understanding is that MN may contribute to evolution throughout life processes of organisms.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144861918","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":"IPSC-Derived Conditioned Medium Reduces Oxidative Stress and Vascular Remodeling in Rat Models of Pulmonary Arterial Hypertension","authors":"Chin-Chang Cheng,&nbsp;Lee-Fen Hsu,&nbsp;Hsien-Hui Chung,&nbsp;Chiang-Wen Lee,&nbsp;Cheng-Hung Chiang,&nbsp;Hung-Chou Yang,&nbsp;Miao-Ching Chi,&nbsp;Ming-Hsueh Lee,&nbsp;Wei-Chun Huang,&nbsp;Pei-Ling Chi","doi":"10.1002/jcp.70085","DOIUrl":"https://doi.org/10.1002/jcp.70085","url":null,"abstract":"<div>\u0000 \u0000 <p>Pulmonary arterial hypertension (PAH) is a progressive vascular disease characterized by elevated pulmonary vascular resistance, leading to right ventricular (RV) hypertrophy and eventual heart failure. Although current therapies provide symptomatic relief, they offer limited efficacy in reversing the underlying vascular remodeling. In this preclinical study, we investigated the therapeutic potential of induced pluripotent stem cell-derived conditioned medium (iPSC-CM) in a monocrotaline (MCT)-induced rat model of PAH, employing both prophylactic and therapeutic administration strategies. iPSC-CM treatment significantly reduced right ventricular systolic pressure (RVSP) and mitigated RV hypertrophy compared to MCT-only controls. Histological analyses revealed attenuated pulmonary arterial wall thickening and muscularization. At the molecular level, iPSC-CM downregulated the expression of hypoxia-inducible factor 1-alpha (HIF-1α) and platelet-derived growth factor-BB (PDGF-BB) in lung tissues, and modulated oxidative stress by decreasing NADPH oxidase 1 (Nox1) and increasing superoxide dismutase 1 (SOD1) levels. In vitro, iPSC-CM suppressed the proliferation and migration of pulmonary artery smooth muscle cells (PASMCs) under hypoxic and PDGF-BB-stimulated conditions. These findings suggest that iPSC-CM targets key pathogenic pathways involved in vascular remodeling and redox imbalance in PAH. Together, these findings support iPSC-CM as a promising acellular approach for targeting vascular remodeling and oxidative stress in PAH, warranting further investigation toward clinical translation.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858542","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":"Growth Factor Receptor-Binding Protein 10 Promotes High Glucose-Induced H9c2 Cardiomyoblast Apoptosis via Inhibition of the ERK1/2 and JAK2/STAT3 Signaling Pathways","authors":"Yuanyuan Wang,&nbsp;Fangfang Bu,&nbsp;Mi Zhang,&nbsp;Ying Zhang,&nbsp;Yanyan Hu,&nbsp;Lin Liu","doi":"10.1002/jcp.70081","DOIUrl":"https://doi.org/10.1002/jcp.70081","url":null,"abstract":"<div>\u0000 \u0000 <p>Cardiomyocyte apoptosis is crucial in the occurrence of diabetic cardiomyopathy; thus, it is important to elucidate the underlying mechanisms involved in elevated glucose and cardiomyocyte apoptosis. Growth factor receptor-binding protein 10 (Grb10) has been proved to participate in the regulation of cell proliferation, migration, and apoptosis. The purpose of this study was to explore the role of Grb10 in high glucose-induced H9c2 cardiomyoblast apoptosis and investigate the underlying molecular mechanisms. H9c2 cardiomyoblasts were cultured and exposed to an elevated glucose at a level of 33 mM. Grb10 expression was inhibited using small interfering RNA (siRNA), and the activities of ERK1/2 and STAT3 were stimulated by specific activators. Western blot analysis was used to detect the expression levels of Grb10, (phosphorylated) ERK1/2, (phosphorylated) JAK2/STAT3, Bax, Bcl2, and cleaved caspase-3, and the TdT-mediated UTP nick end labeling test was used to measure the apoptosis rate. High glucose treatment in H9c2 cardiomyoblasts led to increased Grb10 expression and cell apoptosis. Grb10-siRNA treatment attenuated high glucose-induced H9c2 cell apoptosis. Furthermore, the repressed activities of ERK1/2 and JAK2/STAT3 signaling pathways induced by high glucose were reversed by Grb10-siRNA treatment. Upregulated ERK1/2 or STAT3 activity partially reversed the apoptosis of H9c2 cardiomyoblast caused by high glucose treatment. Our findings show that Grb10 is involved in high glucose-induced H9c2 cardiomyoblast apoptosis and might exert its apoptosis-promoting role through inhibition of the ERK1/2 and JAK2/STAT3 signaling pathways.</p></div>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"240 8","pages":""},"PeriodicalIF":4.0,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144858543","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}