Frontiers in Molecular Biosciences最新文献

{"title":"Identifying potential biomarkers and molecular mechanisms related to arachidonic acid metabolism in vitiligo.","authors":"Xiaoqing Li, Li Yang, Longfei Zhu, Jingying Sun, Cuixiang Xu, Lijun Sun","doi":"10.3389/fmolb.2025.1536477","DOIUrl":"10.3389/fmolb.2025.1536477","url":null,"abstract":"<p><strong>Background: </strong>Numerous studies have reported that dysregulation of fatty acid metabolic pathways is associated with the pathogenesis of vitiligo, in which arachidonic acid metabolism (AAM) plays an important role. However, the molecular mechanisms of AAM in the pathogenesis of vitiligo have not been clarified. Therefore, we aimed to identify the biomarkers and molecular mechanisms associated with AAM in vitiligo using bioinformatics methods.</p><p><strong>Methods: </strong>The GSE75819 and GSE65127 datasets were used in this study as the training and validation sets, respectively, along with 58 AAM-related genes (AAM-RGs). The differentially expressed genes (DEGs) between the lesional and control groups in the training set were identified through differential expression analysis. A biomarker-based nomogram was constructed to predict the risk of vitiligo.</p><p><strong>Results: </strong>15 overlapping candidate genes were obtained between the DEGs and AAM-RGs. Machine-learning algorithms were used to identify six key genes as <i>PTGDS</i>, <i>PNPLA8</i>, <i>FAAH</i>, <i>ABHD12</i>, <i>PTGS1</i>, and <i>MGLL</i>. In both the training and validation sets, <i>PTGDS</i>, <i>PNPLA8</i>, and <i>MGLL</i>. In both the training and validation sets, <i>PTGDS</i>, <i>PNPLA8</i>, and <i>MGLL</i> were regarded as biomarkers. A nomogram based on these biomarkers showed potential for predicting the risk of vitiligo. Functional enrichment, immune cell infiltration, and regulatory network analyses were used to elucidate the molecular mechanisms.</p><p><strong>Conclusion: </strong>In conclusion, <i>PTGDS</i>, <i>PNPLA8</i>, and <i>MGLL</i> were implicated in AAM to influence the pathogenesis of vitiligo. These findings offer insights into vitiligo treatment, although further research is needed for a comprehensive understanding.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1536477"},"PeriodicalIF":3.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896865/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614471","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRP channels and breast cancer: the role of TRPs in the pathophysiological development.","authors":"Yu Zhang, Yanfeng Yi, Yinghao Shu, Xiaochen Ru, Shuaibing He","doi":"10.3389/fmolb.2025.1528663","DOIUrl":"10.3389/fmolb.2025.1528663","url":null,"abstract":"<p><p>TRP channels play important roles in regulating various physiological and pathological processes, including the progression of cancer. Several TRP channels mediate tumour development. This review focuses on the role of TRP channels in the development of breast cancer, including their involvement in proliferation, apoptosis, autophagy, metastasis, and angiogenesis. TRP channels are associated with breast carcinogenesis and their role as potential therapeutic targets and prognostic biomarkers is under investigation. This review summarizes the reported effects of inhibiting or agonizing various TRP channel in breast cancer cells. Although there are relatively mature protocols for the treatment of breast cancer, its treatment is not currently a breakthrough, and therapies targeting TRP channels may be a developable strategy for it.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1528663"},"PeriodicalIF":3.9,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11896876/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143614484","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Jianpi Yangzheng Xiaozheng granule induced ferroptosis to suppress gastric cancer progression through reprogramming lipid metabolism via SCD1/Wnt/β-catenin axis.","authors":"Xiangyang Wang, Jingxiao Li, Rong Qin, Yi Yin, Jiepin Li, Sitian Lin, Xi Zou","doi":"10.3389/fmolb.2025.1523494","DOIUrl":"10.3389/fmolb.2025.1523494","url":null,"abstract":"<p><p>The incidence of Poorly cohesive carcinoma (PCC) has steadily risen in recent years, posing a significant clinical challenge. To reveal the anti-tumor effects of Jianpi Yangzheng Xiaozheng granule (JPYZXZ) in PCC, an initial investigation was performed using CCK-8, colony formation, scratch, and transwell assays. This was followed by network pharmacology studies to gain a deeper understanding of JPYZXZ's impact on gastric cancer (GC). Then reactive oxygen species (ROS), Fe²⁺, malondialdehyde (MDA), glutathione (GSH), Oil Red O staining, BODIPY493/503, triglyceride (TG), and cholesterol (TC) assay kits and western blot (Wb) analysis were applied to exam the regulatory effects of JPYZXZ on ferroptosis and lipid metabolism. Additionally, molecular docking studies and Wb analysis were used to further investigate the mechanisms of JPYZXZ on PCC. Finally, <i>in vivo</i> animal studies were conducted. The results show that JPYZXZ can inhibit the proliferation and migration of PCC cell. It increases the levels of ROS, Fe²⁺, MDA, while declining the content of GSH, TC, TG, and lipid droplet accumulation within cellular compartments. Wb indicates that JPYZXZ can negatively regulate the expression of proteins, including glutathione peroxidase 4 (GPX4), cystine/glutamate antipoter SLC7A11 (xCT), fatty acid synthase (FASN), and acetyl coenzyme A carboxylase 1 (ACC1). Furthermore, ferrostatin-1 (fer-1) is able to reverse the effects of JPYZXZ on the aforementioned markers of ferroptosis and lipid metabolism. Molecular docking analyses reveal that JPYZXZ exhibits a favorable binding affinity towards Stearoyl-Coenzyme A desaturase 1 (SCD1). Mechanism studies demonstrate that JPYZXZ is capable of down-regulating the expressions of proteins like SCD1, β-catenin, GPX4, and xCT, which is analogous to the effects of SCD1 knockdown and the application of SCD1 inhibitor A939572. Nevertheless, when SCD1 is knocked down, JPYZXZ is unable to further downregulate the expressions of these proteins. Animal studies have corroborated the <i>in vitro</i> tumor-inhibiting effects of JPYZXZ. Therefore, this study offers the first evidence that JPYZXZ inhibits PCC progression by orchestrating ferroptosis and altering lipid metabolism, mediated by the SCD1/Wnt/β-catenin pathway.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1523494"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604515","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Structural insights into SOD1: from in silico and molecular dynamics to experimental analyses of ALS-associated E49K and R115G mutants.","authors":"Seyed Mahdi Hosseini Faradonbeh, Bagher Seyedalipour, Nasrin Keivan Behjou, Kimiya Rezaei, Payam Baziyar, Saman Hosseinkhani","doi":"10.3389/fmolb.2025.1532375","DOIUrl":"10.3389/fmolb.2025.1532375","url":null,"abstract":"<p><p>Protein stability is a crucial characteristic that influences both protein activity and structure and plays a significant role in several diseases. Cu/Zn superoxide dismutase 1 (SOD1) mutations serve as a model for elucidating the destabilizing effects on protein folding and misfolding linked to the lethal neurological disease, amyotrophic lateral sclerosis (ALS). In the present study, we have examined the structure and dynamics of the SOD1 protein upon two ALS-associated point mutations at the surface (namely, E49K and R115G), which are located in metal-binding loop IV and Greek key loop VI, respectively. Our analysis was performed through multiple algorithms on the structural characterization of the hSOD1 protein using computational predictions, molecular dynamics (MD) simulations, and experimental studies to understand the effects of amino acid substitutions. Predictive results of computational analysis predicted the deleterious and destabilizing effect of mutants on hSOD1 function and stability. MD outcomes also indicate that the mutations result in structural destabilization by affecting the increased content of β-sheet structures and loss of hydrogen bonds. Moreover, comparative intrinsic and extrinsic fluorescence results of WT-hSOD1 and mutants indicated structural alterations and increased hydrophobic surface pockets, respectively. As well, the existence of β-sheet-dominated structures was observed under amyloidogenic conditions using FTIR spectroscopy. Overall, our findings suggest that mutations in the metal-binding loop IV and Greek key loop VI lead to significant structural and conformational changes that could affect the structure and stability of the hSOD1 molecule, resulting in the formation of toxic intermediate species that cause ALS.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1532375"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial: Machine learning in computer-aided drug design.","authors":"Ognjen Perišić, Cigdem Sevim Bayrak, Mohamed Khaled Gunady","doi":"10.3389/fmolb.2025.1568437","DOIUrl":"10.3389/fmolb.2025.1568437","url":null,"abstract":"","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1568437"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11894378/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604512","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Development of an enzyme-linked immunosorbent assay (ELISA) for determining neutrophil elastase (NE) - a potential useful marker of multi-organ damage observed in COVID-19 and post-Covid-19 (PCS).","authors":"Joanna Adamiec-Mroczek, Joanna Kluz, Sandra Chwałek, Maciej Rabczyński, Kinga Gostomska-Pampuch, Łukasz Lewandowski, Marta Misiuk-Hojło, Beata Ponikowska, Goutam Chourasia, Ilias Dumas, Andrzej Gamian, Żanna Fiodorenko-Dumas, Bogusława Konopska, Agnieszka Gola, Klaudia Konikowska, Daniel Strub, Agnieszka Bronowicka-Szydełko, Katarzyna Madziarska","doi":"10.3389/fmolb.2025.1542898","DOIUrl":"10.3389/fmolb.2025.1542898","url":null,"abstract":"<p><strong>Background: </strong>The ongoing post-COVID-19 syndrome (PCS) epidemic, causing complications of diverse etiology, necessitates the search for new diagnostic markers and the development of widely accessible methods for their detection. This would enable the prognosis of PCS progression and faster implementation of targeted treatments. One potential marker is neutrophil elastase (NE), whose elevated levels in the blood during PCS may result from organ damage caused by increased secretion of severe inflammatory mediators or amyloidosis resulting from the interaction of NE with SARS-CoV-2. The aim of this publication is to present a step-by-step method for designing an enzymatic ELISA test, enabling the quantitative assessment of NE in the blood serum of patients.</p><p><strong>Methods: </strong>NE was measured using the designed ELISA test.</p><p><strong>Results: </strong>The study outlines all the steps necessary for designing and optimizing the ELISA test, including the selection of standards, primary and secondary antibodies, and their dilutions. Using the test, elevated NE levels were demonstrated in patients with advanced-stage diabetic nephropathy after symptomatic COVID-19, compared to a relative group of patients sampled before COVID-19.</p><p><strong>Conclusion: </strong>The undertaken efforts enabled the development of a test with high performance parameters (initially set sensitivity: ≥40 pg/μL; intra-assay precision: 7%; inter-assay precision <20%). No significant cross-reactivity with other tested proteins was observed. Serial dilution of plasma samples resulted in a proportional decrease in signal intensity.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1542898"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893405/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604509","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum: Role of ARRB1 in prognosis and immunotherapy: a pan-cancer analysis.","authors":"Yingquan Ye, Haili Jiang, Yue Wu, Gaoxiang Wang, Yi Huang, Weijie Sun, Mei Zhang","doi":"10.3389/fmolb.2025.1577764","DOIUrl":"https://doi.org/10.3389/fmolb.2025.1577764","url":null,"abstract":"<p><p>[This corrects the article DOI: 10.3389/fmolb.2022.1001225.].</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1577764"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893980/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604505","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Q-Der: a next-generation CoQ10 analogue supercharging neuroprotection by combating oxidative stress and enhancing mitochondrial function.","authors":"Matteo Micucci, Federico Gianfanti, Sabrina Donati Zeppa, Giosuè Annibalini, Barbara Canonico, Fabiana Fanelli, Roberta Saltarelli, Riham Osman, Mariele Montanari, Daniele Lopez, Gemma Nasoni, Giovanna Panza, Erik Bargagni, Francesca Luchetti, Michele Retini, Michele Mari, Giovanni Zappia, Vilberto Stocchi, Alessia Bartolacci, Sabrina Burattini, Michela Battistelli","doi":"10.3389/fmolb.2025.1525103","DOIUrl":"10.3389/fmolb.2025.1525103","url":null,"abstract":"<p><strong>Background: </strong>Mitochondrial dysfunction and oxidative stress are central mechanisms in the progression of neurodegenerative diseases. This study first evaluated the toxicity of Q-Der (Q10-diacetate), a derivative of Coenzyme Q10, in HT22 hippocampal neurons under normal and oxidative stress conditions.</p><p><strong>Methods: </strong>HT22 cells were treated with Q-Der at 2.5, 5 and 10 µM with and without rotenone. Mitochondrial superoxide production (Mitosox), gene expression (via qRT-PCR), and protein levels (via Western blot) were measured. Morphological analyses were performed using transmission (TEM) and scanning (SEM) electron microscopes.</p><p><strong>Results: </strong>Q-Der significantly reduced mitochondrial superoxide levels, particularly at 5 μM, and upregulated key mitochondrial biogenesis genes, including PGC-1α and TFAM. Additionally, it restored the expression of MT-ND1 and MT-COI, which were downregulated by rotenone. Western blot results showed a significant recovery in CV-ATP5A (complex V) expression (p < 0.05), preserving mitochondrial ATP production. Morphological analyses further confirmed Q-Der's ability to maintain cellular and mitochondrial structure under stress conditions.</p><p><strong>Conclusion: </strong>These findings suggest that Q-Der is non-toxic under normal conditions and protects against oxidative stress, supporting its potential as a therapeutic agent for neurodegenerative diseases.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1525103"},"PeriodicalIF":3.9,"publicationDate":"2025-02-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11893404/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143604455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of extracellular vesicles derived from oral squamous cell carcinoma on the metabolic profile of oral fibroblasts.","authors":"Aleksandra Lipka, Tine M Søland, Anni I Nieminen, Dipak Sapkota, Trude M Haug, Hilde K Galtung","doi":"10.3389/fmolb.2025.1492282","DOIUrl":"10.3389/fmolb.2025.1492282","url":null,"abstract":"<p><strong>Introduction: </strong>Oral cancer is one of the most common forms of head and neck cancers. Oral squamous cell carcinoma (OSCC) accounts for more than 90% of the oral malignancies. The molecular pathogenesis of OSCC is complex as it involves altered expression of specific genes and proteins, but also comprises changes in metabolic processes. It is suggested that extracellular vesicles (EVs) released by cancer cells may contribute to cancer development and metastasis by recruiting and changing phenotype of normal cells that surround the tumor.</p><p><strong>Methods: </strong>The aim of the project was to characterize the effect of OSCC EVs on the metabolic profile of normal oral fibroblasts (NOFs). Targeted liquid chromatography mass spectrometry metabolic profiling was performed on control cells and NOFs exposed to OSCC EVs for 24 and 48 h.</p><p><strong>Results: </strong>Analysis of detected metabolites revealed that OSCC EVs affected NOFs the most after 24 h of exposure. Among metabolites that were significantly altered at 24 h, pyruvate, ATP, UTP, coenzyme A, and dihydroxyacetone phosphate were upregulated, while fatty acids such as nervonic acid, linoleate, oleate, palmitoleic acid, and docosahexaenoic acid were downregulated. These findings were supported by Western blotting of pyruvate kinase M2 (PKM2) and aldolase, fructose-bisphosphate A (ALDOA).</p><p><strong>Conclusion: </strong>The metabolic pathways of glycolysis, citric acid cycle, and amino acid metabolism were enriched, suggesting that OSCC EVs cause phenotype switch in NOFs that may contribute to acquiring a pro-tumorigenic phenotype.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1492282"},"PeriodicalIF":3.9,"publicationDate":"2025-02-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11885147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143585114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Two sides of the same coin: heat shock proteins as biomarkers and therapeutic targets for some complex diseases.","authors":"Xolani Henry Makhoba","doi":"10.3389/fmolb.2025.1491227","DOIUrl":"10.3389/fmolb.2025.1491227","url":null,"abstract":"<p><p>Heat shock proteins are molecular chaperones that play crucial roles in the folding and unfolding of complex polypeptides within the cellular system. These molecules are involved in various processes, including vesicular transport, prevention of protein aggregation in the cytosol, and cell signaling. They are also linked to autoimmunity, infection immunity, and tumor immunology. Stressors like heat shock, exposure to heavy metals, cytokines, reactive oxygen species, inflammation, and viruses can influence the production of these molecules. In complex diseases such as cancer, malaria, and COVID-19, heat shock proteins are considered both biomarkers and drug targets. The upregulation of small heat shock proteins like hsp27 and major heat shock proteins 70/90 has been recognized as crucial biomarkers and therapeutic targets for cancer. Additionally, it has been reported that the invasion of <i>Plasmodium falciparum</i>, the causative agent of malaria, leads to the upregulation of heat shock proteins such as hsp40, hsp70, and hsp90. This sudden increase is a protective mechanism from the human host and enhances the parasite's growth, making these proteins significant as biomarkers and malarial drug targets. The presence of the SARS-CoV-2 virus in the human cellular system correlates with a substantial increase in heat shock protein 70 production from host cells. Furthermore, our research group has demonstrated that SARS-CoV-2 hijacks the host's heat shock proteins, and we are currently developing tools to prevent the virus from utilizing the host's protein folding system. This review aims to highlight the role of heat shock proteins as biomarkers and therapeutic targets for selected refractory diseases, focusing on cancer, malaria, and COVID-19. A fundamental molecular docking study was performed to investigate the interaction between a non-structural complex from SARS-CoV-2 and chosen small molecules, which is emphasized in this review.</p>","PeriodicalId":12465,"journal":{"name":"Frontiers in Molecular Biosciences","volume":"12 ","pages":"1491227"},"PeriodicalIF":3.9,"publicationDate":"2025-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882428/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}