Journal of Cellular Physiology最新文献

{"title":"Hematopoietic Stem Cell Tropism Mediated Targeting of Breast Cancer Stem Cells via Alteration of Tumor Immune-Microenvironment.","authors":"Sumit Mallick, Siddhartha Biswas, Sudheer Shenoy P, Bipasha Bose","doi":"10.1002/jcp.70179","DOIUrl":"https://doi.org/10.1002/jcp.70179","url":null,"abstract":"<p><p>The ontogenic development of hematopoietic stem cells (HSCs) occurs across diverse niches, with HSCs migrating from the aorta-gonad-mesonephros (AGM) to the fetal liver and finally residing in the bone marrow after birth, where adult HSCs replenish the hematopoietic system. The HSC niche critically regulates tropism and proliferation via factors secreted by the microenvironment interaction. Here, we hypothesized that HSCs display tropism toward the aggressive cancer stem cell (CSC) niches of triple-negative breast cancer (TNBC) and MCF-7 cells breast cancer, which exhibit high relapse rates and are potential targets for cell therapy. Our results demonstrate HSC-specific tropism toward breast CSCs, leading to interactions that trigger HSC differentiation into CD4⁺ and CD8⁺ subpopulations within the cancer microenvironment. Proteomics of migrated HSCs toward TNBC-CSCs/MCF-7 cells revealed significant upregulation of IL-7, Notch, and other proteins involved in T cell activation and migration pathways. Metabolomics of HSC-conditioned medium (HSC-CM)-treated CSCs/MCF-7 cells further demonstrated that HSC-CM arrests TNBC-CSC growth and cell cycle progression by altering the mitochondrial bioenergetics. This study highlights the potential of leveraging both HSCs and HSC-derived factors for personalized therapies targeting CSCs in TNBC.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 5","pages":"e70179"},"PeriodicalIF":4.0,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147838476","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":"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":"https://doi.org/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":"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":"https://doi.org/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":"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":"https://doi.org/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":"Rh3R Attenuates RANKL-Induced Osteoclast Differentiation and F-Actin Ring Formation via the Suppression of c-Fos/NFATc1 Signaling in Primary Murine Cells.","authors":"Hyung-Mun Yun, Soo Hyun Kim, Joonyeop Lee, Kyung-Ran Park","doi":"10.1002/jcp.70174","DOIUrl":"https://doi.org/10.1002/jcp.70174","url":null,"abstract":"<p><p>The homeostatic balance of bone remodeling is governed by the precise coordination between bone-forming osteoblasts and bone-resorbing osteoclasts. In this study, we investigated the anti-resorptive properties of rhamnocitrin-3-rhamnoside (Rh3R), a flavonoid isolated from Loranthus tanakae, using primary bone marrow-derived macrophages (BMMs) and calvaria-derived osteogenic progenitor cells (COCs) to ensure biological relevance. Our findings demonstrate that Rh3R potently inhibits the RANKL-induced differentiation of BMMs into TRAP-positive multinucleated osteoclasts in a dose-dependent manner, without inducing cytotoxicity. Mechanistically, Rh3R effectively attenuates RANKL-induced downstream signaling cascades, as evidenced by the attenuated phosphorylation of MAPKs (ERK1/2, JNK, p38), AKT, and IκB. This signaling blockade subsequently suppresses the induction of the master transcription factors, c-Fos and NFATc1. Furthermore, Rh3R impairs the functional resorptive capacity of mature osteoclasts by destabilizing F-actin-rich ring structures accompanied by decreased integrin β3 expression, thereby preventing the formation of a functional sealing zone. The inhibitory effect of Rh3R on bone-degrading activity was further confirmed by a significant reduction in the total area of resorption pits on bone slices. Notably, Rh3R exhibits a lineage-specific inhibitory effect, showing no adverse influence on osteoblastogenesis or the mineralizing capacity of primary osteogenic cells. Furthermore, the effect of Rh3R was consistently maintained in a co-culture system of primary osteoblasts and BMMs. Collectively, these in vitro findings identify Rh3R as a bioactive modulator of osteoclast differentiation and function via suppression of RANKL-induced downstream signaling, warranting future in vivo and pharmacological studies to evaluate efficacy, exposure, and safety.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70174"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690334","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: Exosome-Encapsulated miR-6089 Regulates Inflammatory Response via Targeting TLR4.","authors":"","doi":"10.1002/jcp.70170","DOIUrl":"https://doi.org/10.1002/jcp.70170","url":null,"abstract":"<p><p>RETRACTION: \"Exosome-Encapsulated miR-6089 Regulates Inflammatory Response via Targeting TLR4,\" by D. Xu, M. Song, C. Chai, H. et al., Journal of Cellular Physiology 234, no. 2 (2019): 1502-1511, https://doi.org/10.1002/jcp.27014. The above article, published online on 21 August 2018 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 third parties. Specifically, image elements in Figure 4F were found to have been previously published by the author group in a different scientific context. Furthermore, scientific inconsistencies were identified that undermine the study's rationale, and the article lacks essential information required to interpret and reproduce the findings. The authors did not respond to our request for comments. Accordingly, the article has been retracted as the editors have lost confidence in the accuracy and integrity of the whole body of data and consider the conclusions of the article invalid. The authors were informed of the retraction decision but were unavailable for final confirmation.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70170"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147690415","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":"Novel Regulatory Cell Death in Intervertebral Disc Degeneration.","authors":"Xianxu Zhang, Zixian Liu, Yuhao Chen, Fanyu Bai, Yizhi Zhang, Mingchun Li, Shishun Yan, Zhiqiang Luo, Mingcong Ding","doi":"10.1002/jcp.70180","DOIUrl":"https://doi.org/10.1002/jcp.70180","url":null,"abstract":"<p><p>Intervertebral disc degeneration (IDD) is a major cause of chronic low back pain. Its pathogenesis is highly complex and encompasses multiple pathological processes, including cellular dysfunction, extracellular matrix (ECM) degradation, inflammatory responses, oxidative stress, and aberrant mechanical loading. Traditionally, programmed cell death (PCD), particularly apoptosis and autophagy, has been regarded as a key contributor to IDD. However, with ongoing advances in this field, an expanding number of emerging forms of regulated cell death (RCD) have been identified and demonstrated to play critical roles in the initiation and progression of IDD. These advances have also provided new insights into the key molecular events underlying disc degeneration and have facilitated the identification of potential disease-modifying therapeutic targets. This review systematically summarizes five emerging RCD modalities, namely ferroptosis, cuproptosis, necroptosis, PANoptosis, and disulfidptosis, with particular emphasis on their mechanistic roles, key regulatory factors, signaling pathways, and patterns of interaction in IDD. Current evidence indicates that these RCD modalities not only independently contribute to cell death but may also converge through shared pathological nodes, including oxidative stress, mitochondrial dysfunction, and inflammatory signaling, thereby producing synergistic amplification effects that further aggravate cell loss and matrix destruction. Regarding therapeutic strategies, a range of RCD-targeted pharmacological approaches has been reported to exhibit potential therapeutic value, including iron chelators, modulators of copper metabolism, inhibitors of the RIPK signaling pathway, antioxidants, and agents targeting PANoptosis-related signaling. These findings provide novel perspectives for the precision treatment of IDD. Nevertheless, most available studies remain limited to cellular and animal models, and the spatiotemporal expression patterns of the relevant signaling networks, their mechanisms of interaction, and their dynamic changes across different stages of degeneration remain to be further elucidated. Taken together, the identification of emerging RCD mechanisms has provided a more comprehensive framework for understanding the complex pathological processes of IDD. Furthermore, it has established a theoretical basis for the development of multi-target combinatorial intervention strategies and disease-modifying therapeutic paradigms, and may ultimately facilitate a shift in IDD management from symptomatic relief alone toward etiology-oriented and precision-based interventions.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70180"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147772627","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":"Reversible Nucleolar Stress and Cell Growth Arrest Triggered by Acidic pH.","authors":"Carulina Bueno de Mesquita, Atsushi Kaida, Hitomi Nojima, Masahiko Miura","doi":"10.1002/jcp.70176","DOIUrl":"10.1002/jcp.70176","url":null,"abstract":"<p><p>The tumor microenvironment is often characterized by hypoxia and extracellular acidosis, which modulate various tumor cell phenotypes. Ribosome biogenesis is a highly energy-demanding process that is essential for protein synthesis and cell proliferation and is sensitive to cellular stress, resulting in a nucleolar stress response. However, whether extracellular acidosis impairs ribosome biogenesis and induces nucleolar stress remains unclear. In this study, we demonstrated that an acidic pH downregulates ribosome biogenesis in cancer cells. RNA sequencing revealed the downregulation of genes related to ribosome biogenesis and cell cycle progression under acidic conditions. Consistently, acidic pH reduced the pre-rRNA levels and induced nucleolar stress, as evidenced by NPM1 translocation from the nucleolus to the nucleoplasm, which led to G1 phase arrest and growth inhibition. Importantly, these effects were reversed upon restoration of neutral pH, with recovery of pre-rRNA expression, NPM1 localization, and cell proliferation. Further, an acidic pH shifted the intracellular redox balance toward an oxidized state. Treatment with the reductant dithiothreitol partially reversed NPM1 translocation, suggesting that oxidative stress contributes, at least partially, to the nucleolar stress response. Overall, our findings reveal a previously unrecognized link between extracellular acidosis and impaired ribosome biogenesis, leading to nucleolar stress and reversible growth arrest. This acidosis-driven stress response represents a therapeutic vulnerability in solid tumors, offering a novel strategy to overcome treatment resistance associated with the acidic tumor microenvironment.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70176"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13088739/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698962","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":"Impact of Maternal Supraphysiological Hypercholesterolemia on Lysosomal and Mitochondrial Function in Placental Trophoblast Cells.","authors":"María José Yañez, Fabián Campos, Patricia Valdebenito, Viviana A Cavieres, María José Barrera, Cheril Tapia-Rojas, Patricia V Burgos, Lara J Monteiro, Silvana Zanlungo, Sebastián E Illanes, Andrea Leiva","doi":"10.1002/jcp.70165","DOIUrl":"https://doi.org/10.1002/jcp.70165","url":null,"abstract":"<p><p>Dyslipidemia, characterized by an excessive amount of lipids in the bloodstream, is a significant risk factor for metabolic disorders and cardiovascular diseases (CVDs). Maternal supraphysiological hypercholesterolemia (MSPH) is associated with increased maternal levels of total cholesterol (TC) and low-density lipoprotein (LDL). This condition has been linked to negative consequences on the fetoplacental vasculature, including increased atherosclerosis development in the fetal aorta and later in children and adolescents. This study aims to determine whether the high cholesterol levels associated with MSPH affect lysosomal and mitochondrial functions in the syncytiotrophoblast (STB), considering the increased free cholesterol levels previously reported in primary human trophoblast (PHT) cells from MSPH pregnancies. Total cholesterol levels were measured in placental tissues and BeWo cells. Lysosomal mass, size, and activity, as well as mitochondrial mass, function, and morphology, were assessed in BeWo cells and placentas. Our results revealed that placental tissues from MSPH pregnancies and BeWo cells treated with oxidized (ox-LDL) exhibited increased free cholesterol levels and higher expression of cholesterol transport proteins. Treatment of BeWo cells with ox-LDL also led to an increase in lysosomal mass and size, accompanied by a decrease in lysosomal activity. Conversely, ox-LDL treatment induced mitochondrial fragmentation in BeWo cells, together with reduced ATP production and diminished mitochondrial membrane potential. Similar alterations in lysosomes and mitochondria were observed in the placenta of patients with a history of MSPH. MSPH-related high cholesterol levels induced by ox-LDL impair lysosomal and mitochondrial functions in the STB, potentially contributing to cellular dysfunction observed in MSPH. This study highlights the importance of understanding the underlying mechanisms of MSPH to improve maternal and fetal health outcomes.</p>","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70165"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147622975","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":"Correction to \"FGF21 Impedes Peripheral Myelin Development by Stimulating p38 MAPK/c-Jun Axis\".","authors":"","doi":"10.1002/jcp.70158","DOIUrl":"https://doi.org/10.1002/jcp.70158","url":null,"abstract":"","PeriodicalId":15220,"journal":{"name":"Journal of Cellular Physiology","volume":"241 4","pages":"e70158"},"PeriodicalIF":4.0,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147698967","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}