Cells最新文献

{"title":"Neutralizing IL-15 Inhibits Tissue-Damaging Immune Response in Ex Vivo Cultured Untreated Celiac Intestinal Mucosa.","authors":"Vera Rotondi Aufiero, Giuseppe Iacomino, Giovanni De Chiara, Errico Picariello, Gaetano Iaquinto, Riccardo Troncone, Giuseppe Mazzarella","doi":"10.3390/cells14030234","DOIUrl":"10.3390/cells14030234","url":null,"abstract":"<p><p>In celiac disease (CeD), interleukin 15 (IL-15) affects the epithelial barrier by acting on intraepithelial lymphocytes, promoting interferon γ (IFN-γ) production and inducing strong cytotoxic activity as well as eliciting apoptotic death of enterocytes by the Fas/Fas ligand system. This study investigates the effects of a monoclonal antibody neutralizing the effects of IL-15 (aIL-15) on tissue-damaging immune response in untreated CeD patients by using an organ culture system. Jejunal biopsies from 10 untreated CeD patients were cultured ex vivo with or without aIL-15. Epithelial expressions of CD95/Fas, HLA-E and perforin were analyzed by immunohistochemistry. Apoptosis was detected in the epithelium by using the terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) assay. Additionally, the surface epithelium compartment of ex vivo cultured biopsy samples was isolated by laser capture microdissection (LCM). RNA from each LCM sample was extracted and the relative expression of IFN-γ was evaluated by quantitative reverse transcriptase-PCR (qRT-PCR). Biopsies cultured with the aIL-15 antibody showed a reduction in Fas, HLA-E and perforin epithelial expression, as well as a decrease in epithelial TUNEL+ cells compared to biopsies cultured without the aIL-15 antibody. Moreover, downregulation of epithelial IFN-γ expression was recorded in biopsies incubated with aIL-15, compared to those cultured without aIL-15. Our findings suggest that neutralizing the effects of IL-15 in ex vivo cultured untreated CeD intestinal mucosa could block apoptosis by downregulating Fas and HLA-E expression and the release of cytotoxic proteins, such as perforin. Furthermore, it can dampen the hyperactive immune response by reducing IFN-γ expression. More generally, our study provides new evidence for the effects of anti-IL-15 neutralizing monoclonal antibodies in preventing or repairing epithelial damage and further supports the concept that IL-15 is a meaningful therapeutic target in CeD, or inflammatory diseases associated with the upregulation of IL-15.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11818035/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398412","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":"Regulatory Elements for Gene Therapy of Epilepsy.","authors":"Ekaterina Chesnokova, Natalia Bal, Ghofran Alhalabi, Pavel Balaban","doi":"10.3390/cells14030236","DOIUrl":"10.3390/cells14030236","url":null,"abstract":"<p><p>The problem of drug resistance in epilepsy means that in many cases, a surgical treatment may be advised. But this is only possible if there is an epileptic focus, and resective brain surgery may have adverse side effects. One of the promising alternatives is gene therapy, which allows the targeted expression of therapeutic genes in different brain regions, and even in specific cell types. In this review, we provide detailed explanations of some key terms related to genetic engineering, and describe various regulatory elements that have already been used in the development of different approaches to treating epilepsy using viral vectors. We compare a few universal promoters for their strength and duration of transgene expression, and in our description of cell-specific promoters, we focus on elements driving expression in glutamatergic neurons, GABAergic neurons and astrocytes. We also explore enhancers and some other cis-regulatory elements currently used in viral vectors for gene therapy, and consider future perspectives of state-of-the-art technologies for designing new, stronger and more specific regulatory elements. Gene therapy has multiple advantages and should become more common in the future, but there is still a lot to study and invent in this field.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816724/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398216","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":"Intermittent Overconsumption of High Fat Diet Promotes Microglial Reactivity in the Hypothalamus and Hindbrain of Female Rats.","authors":"Alexis A Campanile, Lisa A Eckel","doi":"10.3390/cells14030233","DOIUrl":"10.3390/cells14030233","url":null,"abstract":"<p><p>Elevated proinflammatory cytokines were reported in binge eating spectrum disorders characterized by intermittent overconsumption during periods of otherwise normal or restricted food intake. It is unknown whether binge eating promotes neuroinflammation, similar to that observed following chronic overconsumption of a high fat diet (HFD) in rodents. Here, we used a rodent model of binge-like eating to test the hypothesis that intermittent overconsumption of HFD promotes microglial reactivity in brain areas that control food intake. To promote overconsumption, one group of rats received chow plus intermittent access to HFD (INT). Control groups received either chow only (CHOW) or chow plus continuous access to HFD (CONT). Following behavioral testing, brains were processed to visualize ionized calcium-binding adaptor molecule 1 (Iba1), a microglial marker. INT rats consumed more calories than the control rats on days when the HFD was available, and fewer calories than the control rats on days when they only had access to chow. Despite consuming fewer total calories and 50% fewer fat calories, lean INT rats developed a pattern of microglial reactivity in feeding-relevant brain areas similar to obese CONT rats. We conclude that intermittent overconsumption of HFD, without diet-induced weight gain, promotes microglial reactivity in brain regions that control feeding.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817838/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398317","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":"Magnetically Stimulated Myogenesis Recruits a CRY2-TRPC1 Photosensitive Signaling Axis.","authors":"Jan Nikolas Iversen, Yee Kit Tai, Kwan Yu Wu, Craig Jun Kit Wong, Hao Yang Lim, Alfredo Franco-Obregón","doi":"10.3390/cells14030231","DOIUrl":"10.3390/cells14030231","url":null,"abstract":"<p><p>The cryptochromes are flavoproteins that either individually or synergistically respond to light and magnetic field directionality as well as are implicated in circadian rhythm entrainment and development. Single brief exposures (10 min) to low energy (1.5 mT) pulsed electromagnetic fields (PEMFs) were previously shown to enhance myogenesis by stimulating transient receptor potential canonical 1 (TRPC1)-mediated Ca²⁺ entry, whereby downwardly directed fields produced greater myogenic enhancement than upwardly directed fields. Here, we show that growth in the dark results in myoblasts losing their sensitivity to both magnetic field exposure and directionality. By contrast, overexpressing or silencing cryptochrome circadian regulator 2 (CRY2) in myoblasts enhances or reduces PEMF responses, respectively, under conditions of ambient light. Reducing cellular flavin adenine dinucleotide (FAD) content by silencing riboflavin kinase (RFK) attenuated responsiveness to PEMFs and inhibited selectivity for magnetic field direction. The upregulation of TRPC1 and cell cycle regulatory proteins typically observed in response to PEMF exposure was instead attenuated by upwardly directed magnetic fields, growth in the darkness, magnetic shielding, or the silencing of CRY2 or RFK. A physical interaction between CRY2 and TRPC1 was detected using coimmunoprecipitation and immunofluorescence, revealing their co-translocation into the nucleus after PEMF exposure. These results implicate CRY2 in an identified TRPC1-dependent magnetotransduction myogenic cascade.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398396","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":"Comprehensive SUMO Proteomic Analyses Identify HIV Latency-Associated Proteins in Microglia.","authors":"Fergan Imbert, Dianne Langford","doi":"10.3390/cells14030235","DOIUrl":"10.3390/cells14030235","url":null,"abstract":"<p><p>SUMOylation, the post-translational modification of proteins by small ubiquitin-like modifiers, plays a critical role in regulating various cellular processes, including innate immunity. This modification is essential for modulating immune responses and influencing signaling pathways that govern the activation and function of immune cells. Recent studies suggest that SUMOylation also contributes to the pathophysiology of central nervous system (CNS) viral infections, where it contributes to the host response and viral replication dynamics. Here, we explore the multifaceted role of SUMOylation in innate immune signaling and its implications for viral infections within the CNS. Notably, we present novel proteomic analyses aimed at elucidating the role of the small ubiquitin-related modifier (SUMO) in human immunodeficiency virus (HIV) latency in microglial cells. Our findings indicate that SUMOylation may regulate key proteins involved in maintaining viral latency, suggesting a potential mechanism by which HIV evades immune detection in the CNS. By integrating insights from proteomics with functional studies, we anticipate these findings to be the groundwork for future studies on HIV-host interactions and the mechanisms that underlie SUMOylation during latent and productive infection.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817477/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397957","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":"Fabry Disease and Inflammation: Potential Role of p65 iso5, an Isoform of the NF-κB Complex.","authors":"Giuseppa Biddeci, Gaetano Spinelli, Paolo Colomba, Giovanni Duro, Monia Anania, Daniele Francofonte, Francesco Di Blasi","doi":"10.3390/cells14030230","DOIUrl":"10.3390/cells14030230","url":null,"abstract":"<p><p>Fabry disease (FD) is an X-linked lysosomal storage disease, caused by mutations in the <i>GLA</i> gene on the X chromosome, resulting in a deficiency of the lysosomal enzyme α-GAL. This leads to the progressive accumulation of Gb3 in cells, causing multi-systemic effects. FD has been classified as a subgroup of autoinflammatory diseases. NF-κB is a family of ubiquitous and inducible transcription factors that play critical roles in inflammation, in which the p65/p50 heterodimer is the most abundant. The glucocorticoid receptor (GR) represents the physiological antagonists in the inflammation process. A novel spliced variant of p65, named p65 iso5, which can bind the dexamethasone, enhancing GR activity, has been found. This study investigates the potential role of p65 iso5 in the inflammation of subjects with FD. We evaluated in peripheral blood mononuclear cells (PBMCs), from over 100 FD patients, the p65 iso5 mRNA level, and the protein expression. The results showed significantly lower p65 iso5 mRNA and protein expression levels compared to controls. These findings, along with the ability of p65 iso5 to bind dexamethasone and the regulation of the glucocorticoid response in the opposite way of p65, strongly suggest the involvement of p65 iso5 in the inflammatory response in FD.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817417/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398235","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":"Mitochondrial Alterations, Oxidative Stress, and Therapeutic Implications in Alzheimer's Disease: A Narrative Review.","authors":"Erica Spina, Riccardo Rocco Ferrari, Elisa Pellegrini, Mauro Colombo, Tino Emanuele Poloni, Antonio Guaita, Annalisa Davin","doi":"10.3390/cells14030229","DOIUrl":"10.3390/cells14030229","url":null,"abstract":"<p><p>The relationship between aging, mitochondrial dysfunction, neurodegeneration, and the onset of Alzheimer's disease (AD) is a complex area of study. Aging is the primary risk factor for AD, and it is associated with a decline in mitochondrial function. This mitochondrial dysfunction is believed to contribute to the neurodegenerative processes observed in AD. Neurodegeneration in AD is characterized by the progressive loss of synapses and neurons, particularly in regions of the brain involved in memory and cognition. It is hypothesized that mitochondrial dysfunction plays a pivotal role by disrupting cellular energy metabolism and increasing the production of reactive oxygen species (ROS), which can damage cellular components and exacerbate neuronal loss. Despite extensive research, the precise molecular pathways linking mitochondrial dysfunction to AD pathology are not fully understood. Various hypotheses have been proposed, including the mitochondrial cascade hypothesis, which suggests that mitochondrial dysfunction is an early event in AD pathogenesis that triggers a cascade of cellular events leading to neurodegeneration. With this narrative review, we aim to summarize some specific issues in the literature on mitochondria and their involvement in AD onset, with a focus on the development of therapeutical strategies targeting the mitochondria environment and their potential application for the treatment of AD itself.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817193/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398374","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":"Effect of Neutron Radiation on ¹⁰BPA-Loaded Melanoma Spheroids and Melanocytes.","authors":"Monika Szczepanek, Michał Silarski, Agnieszka Panek, Anna Telk, Katarzyna Dziedzic-Kocurek, Gabriele Parisi, Saverio Altieri, Ewa Ł Stępień","doi":"10.3390/cells14030232","DOIUrl":"10.3390/cells14030232","url":null,"abstract":"<p><p>Melanoma is an aggressive disease that arises from mutations in the cells that produce the pigment melanin, melanocytes. Melanoma is characterized by a high mortality rate, due to avoidance of applied therapies and metastasis to other organs. The peculiar features of boron neutron capture therapy (BNCT), particularly its cell-level selectivity, make BNCT a promising modality for melanoma treatment. However, appropriate cellular models should be used to study new therapies or improve the efficacy of existing therapies. Spheroids, which have been used for years for in vitro studies of the efficacy of anti-cancer therapies, have many characteristics shared with tumors through which they can increase the accuracy of the cellular response compared to 2D culture in vitro studies and reduce the use of animals for research in the future. To the best of our knowledge, when we started researching the use of spheroids in BNCT in vitro, there was no publication showing such use. Our study aimed to evaluate the efficacy of a 3D cellular model (spheroids) for testing BNCT on melanoma cells. We assessed boronophenylalanine (¹⁰BPA) uptake using inductively coupled plasma mass spectrometry in both spheroids and 2D cultures of melanoma and melanocytes. DNA damage, Ki67 protein expression, and spheroid growth were analyzed. The experimental groups included: (1) IR_B (neutron flux + 50 µg ¹⁰B/mL), (2) IR (neutron flux alone), (3) C_B (no irradiation, 50 µg ¹⁰B/mL), and (4) C (no irradiation and no treatment with boron). The total absorbed doses were estimated to be 2.1-3.1 Gy for IR_B cells and spheroids as well as 8.3-9.4 Gy for IR_B spheroids, while estimated doses for IR cells were 0.5-1.9 Gy. The results indicated that IR_B spheroids might exhibit a reduced diameter. Melanoma cells in the 3D model showed that their DNA damage levels may be higher than those in the 2D model. Moreover, the Ki67 assay revealed differences in the expression of this marker between irradiated melanoma cell lines. In conclusion, preincubation with ¹⁰BPA enhances BNCT efficacy, leading to cell growth inhibition and increased DNA fragmentation. Differences in DNA damage between 2D and 3D models may be due to dissimilarities in cell metabolism caused by a changed cell architecture.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398212","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":"The Expression of Neuroendocrine Markers in a Small Subset of Ameloblastoma with Implications of Clusterin.","authors":"Hiromasa Hasegawa, Takanaga Ochiai, Rita R Roy, Katsumitsu Shimada","doi":"10.3390/cells14030224","DOIUrl":"10.3390/cells14030224","url":null,"abstract":"<p><p>Immunohistochemically, ameloblastomas often express CD56; however, novel neuroendocrine markers such as synaptophysin (SYP), insulinoma-associated protein 1 (INSM1), and chromogranin A (CgA) remain unexplored. We analyzed 36 ameloblastoma specimens for CD56, SYP, CgA, and clusterin (CLU) and examined limited samples for INSM1 expression by performing immunohistochemistry, transmission electron microscopy, and reverse transcriptase-polymerase chain reaction. Our findings indicate that the limited cells were positive for CD56, SYP, CgA, INSM1, and CLU expression in 72% (26/36), 14% (5/36), 0% (0/40), 80% (4/5), and 22% (8/36) of the cases, respectively. CD56 expression correlated with older age, but not with subtype, SYP, and CLU expression. However, SYP-positive cases were exclusively found in CD56- and CLU-positive cases, and SYP and CLU expression were significantly correlated. Selected cases had dense-core granules and <i>NCAM1</i> and <i>SYP</i> mRNA expression. This study is the first to suggest neuroendocrine differentiation in ameloblastomas, as indicated by SYP and INSM1 immunoexpression and the presence of dense-core granules, which are consistent with the recent World Health Organization classification of Head and Neck Tumors guidelines. SYP-positive and CgA-negative phenotypes may characterize neuroendocrine differentiation in ameloblastoma. Although the underlying molecular mechanism remains unclear, CLU expression may be associated with neuroendocrine differentiation.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11816440/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398339","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":"The Role of Senescence in Experimental Periodontitis at the Causal Level: An in Vivo Study.","authors":"Xiaogang Chu, Mahmoud Elashiry, Angelica Carroll, Celine Joyce Cornelius Timothius, Christopher W Cutler, Ranya Elsayed","doi":"10.3390/cells14030226","DOIUrl":"10.3390/cells14030226","url":null,"abstract":"<p><p>The occurrence and severity of periodontitis (PD) tend to increase with age, and yet the underlying mechanisms remain unclear. Immune senescence is known to be triggered in mice and humans as they age. Experimental PD in mice has been shown to induce senescence biomarkers p16 ^INK4a and p21, dysfunction of antigen-presenting cells (APCs), and activation of the senescence-associated secretory phenotype (SASP). However, the causal links of senescence to experimental PD are not yet established. This study aims to elucidate the role of senescence in experimental PD at a causal level. The P16-3MR mouse model harbors the p16^INK4a (Cdkn2a) promoter, driving in vivo expression of synthetic Renilla luciferase, monomeric red fluorescent protein (mRFP), and herpes simplex virus-1 thymidine kinase (HSV-TK). This facilitates in vivo identification of p16 ^INK4a activation at the cellular level and the consequences of selective elimination of p16^INK4a-positive cells by ganciclovir (GCV) treatment. Mice were treated with/without GCV for two weeks during ligature-induced PD. In vivo bioluminescence imaging quantified p16^INK4a activation, while Western blot and immunofluorescence analyses assessed key senescence and inflammatory markers (p16, p21, p53, Cyclin D1, p-H2A.X, IL17, and IL1β). Alveolar bone volume was analyzed by micro-CT and histomorphometry. Our findings demonstrate that clearance of senescent cells in mice subjected to experimental PD alleviates inflammation and mitigates bone loss. These results suggest a causal role for senescence in PD pathology, raising the future prospect of senolytic agents for therapeutic intervention in PD.</p>","PeriodicalId":9743,"journal":{"name":"Cells","volume":"14 3","pages":""},"PeriodicalIF":5.1,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11817363/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143398361","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}