Journal of physiology and biochemistry最新文献

{"title":"Interplay between NETosis and the lncRNA-microRNA regulatory axis in the immunopathogenesis of cancer.","authors":"Nisreen Salah Majeed, Mohammed Hashim Mohammed, Zainab Amer Hatem, Amr Ali Mohamed Abdelgawwad El-Sehrawy, Subbulakshmi Ganesan, Abhayveer Singh, Marwa Azeez Akoul, Puneet Sudan, Roshni Singh, Hamad Ali Hamad","doi":"10.1007/s13105-025-01082-x","DOIUrl":"10.1007/s13105-025-01082-x","url":null,"abstract":"<p><p>Neutrophil extracellular traps (NETs), web-like complex structures secreted by neutrophils, have emerged as key players in the modulation of immune responses and the immunopathogenesis of immune disorders. Initially described for their antimicrobial function, NETs now play a part in the fundamental processes of cancer biology, including cancer initiation, metastatic dissemination, and immune evasion strategies. NETs hijack anti-tumor immunity by entrapping circulating cancer cells, fostering the growth of tumors, and reorganizing the tumor microenvironment such that it is pro-malignancy. Emerging evidence emphasizes the role of NETosis coupled with non-coding RNAs-long non-coding RNAs (lncRNAs) and microRNAs (miRNAs)-as key regulators of gene expression and controllers of processes vital for cancer growth, such as immune response and programmed cell death processes like apoptosis, necroptosis, pyroptosis, and ferroptosis. Aberrantly expressed non-coding RNAs have been attributed to immune dysregulation and excessive NET production, promoting tumor growth. NETs are also associated with a myriad of pathological conditions, such as autoimmune disorders, cystic fibrosis, sepsis, and thrombotic disorders. New therapeutic approaches-such as DNase therapy and PAD4 inhibitors-target NET production and their degradation to modify immune function and the efficiency of immunotherapies. Further clarification of the intricate interactions of NETosis, lncRNAs, and miRNAs has the potential to establish new strategies for the suppression of the growth of tumors and preventing immune evasion. This review seeks to elucidate the interactions between NETosis and the regulatory networks involving non-coding RNAs that significantly contribute to the immunopathogenesis of cancer.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"499-520"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144016189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"PLAC8 as a potential therapeutic target for myocardial infarction: unraveling the molecular mechanisms.","authors":"Yifan Tong, Xin Huang, Wei Qian, Lijuan Liu","doi":"10.1007/s13105-025-01098-3","DOIUrl":"10.1007/s13105-025-01098-3","url":null,"abstract":"<p><p>The incidence of myocardial infarction (MI) has been increasing in recent years, and the cause of acute myocardial infarction is apoptosis due to insufficient coronary myocardial blood supply. PLAC8 is a critical gene in the disease process of MI through GEO database research and analysis of differentially expressed genes (DEGs). In this study, in mice with myocardial infarction caused by surgical ligation of the left anterior descending coronary artery (LAD) and hypoxia-induced H9C2 cells as a model, the myocardium of the model group was found to show severe cardiomyocyte disorders, apoptosis of inflammatory cell infiltration, and ischemic state by HE, TTC, and Tunel staining. The expression of PLAC8 was reduced in the disease model by PCR and Western blot, and the expression of cle-Casp3 and Bax was also found to be high. However, overexpression of PLAC8 in the disease model reversed these processes. MEK/ERK and P65 are the core signaling pathways in the MI model. In this study, we found that the therapeutic effect of PLAC8 was related to the inhibition of the MEK/ERK signaling pathway by overexpression of PLAC8 and antagonism of the MEK/ERK signaling pathway. In conclusion, the inhibition of the MEK/ERK signaling pathway by PLAC8 under hypoxic conditions reduces apoptosis in H9c2 cells, which may provide new ideas for the determination and treatment of MI.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"741-750"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373543/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144225787","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":"Alterations in hepatic amino acid metabolism related to MASLD in individuals with obesity.","authors":"Armando J Pérez-Díaz, Inmaculada Ros-Madrid, María A Martínez-Sánchez, Sara Rico-Chazarra, Alba Oliva-Bolarín, Andrés Balaguer-Román, Virginia E Fernández-Ruiz, Carlos M Martínez, José E Yuste, Mercedes Ferrer-Gómez, Camilo J Llamoza-Torres, María D Frutos, María Á Núñez-Sánchez, Bruno Ramos-Molina","doi":"10.1007/s13105-025-01086-7","DOIUrl":"10.1007/s13105-025-01086-7","url":null,"abstract":"<p><p>Deregulation of amino acid (AA) metabolism has been reported in several pathological conditions, including metabolic diseases (e.g., obesity and diabetes), cardiovascular diseases, and cancer. However, the role of alterations in AA levels in chronic liver disorders such as metabolic dysfunction-associated steatotic liver disease (MASLD) remains largely unexplored. In this study we aimed to evaluate the hepatic AA composition in patients with different stages of MASLD, and their relationship with MASLD-related risk factors. A case-control study was conducted in 40 patients with obesity undergoing bariatric surgery at Virgen de la Arrixaca University Hospital (Murcia, Spain), where MASLD diagnosis was confirmed by histological analysis of liver biopsies, and hepatic AA levels were measured using ultra-performance liquid chromatography high-resolution time-of-flight mass spectrometry. Our results revealed that the hepatic AA profile was significantly altered in patients with MASLD. More specifically, comparison between MASLD patients revealed a significant increase in hepatic levels of arginine, glycine and cystine in MASH samples compared to steatotic livers. In addition, hepatic concentrations of arginine, lysine and cystine positively correlated with histopathological diagnosis and other MASLD-related parameters, including transaminases and CK-18 levels. These findings suggest that alterations in certain hepatic AA levels such as arginine, lysine, glycine and cystine in MASLD patients could have translational relevance in understanding the onset of this disease.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"625-634"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144031013","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oleoylethanolamine precursor triggers lipolysis during Time-Restricted Intermittent Fasting and promotes longevity and healthy aging of Caenorhabditis elegans.","authors":"Thondimuthu Vinitha, Rajasekharan Sharika, Krishnaswamy Balamurugan","doi":"10.1007/s13105-025-01087-6","DOIUrl":"10.1007/s13105-025-01087-6","url":null,"abstract":"<p><p>Intermittent fasting (IF), Time-Restricted Intermittent Fasting (TRIF), and fasting-mimicking diets have gained popularity among weight loss programs. The body efficiently utilizes its energy reserves to activate metabolic processes in response to food intake. Modifying food regimens can alter/extend life span and promote healthy aging by activating specific metabolic processes. However, changes in general lipid metabolism, especially the alteration in N-acylethanolamide (NAE) regulation and their role in promoting lipolysis and extending life span during TRIF, are still inadequately explored. To bridge the knowledge gap, this study focuses on enhancing Oleoylethanolamine (OEA), a precursor molecule that instigates satiety, promotes lipolysis and extends the life span of model system, Caenorhabditis elegans. TRIF regimen in C. elegans induces OEA, which in turn lead to satiety followed by lipolysis and ATP synthesis. Lipolysis is stimulated by the increase in Adipose Tissue Triglyceride Lipase-1 (ATGL-1) activity that results from the enrichment in OEA precursor. In addition, the TRIF regimen induces oxidative stress resistance in C. elegans. Subsequently, this promotes longevity and slow aging in C. elegans by altering the insulin/ insulin-like growth factor signaling (IIS) pathway. The present study suggested the beneficial effects of time-restricted fasting in the eukaryotic model nematodes through the activation of lipid metabolism that involves enhanced production of OEA precursors which promotes lipolysis. In addition, the data revealed that the increased ATP production resulted in oxidative stress tolerance that promoted longevity and slow aging processes.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"635-656"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144005948","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"miR-320-3p regulates apelin and TGF-β/SMAD3 signaling in hypobaric hypoxia exposed rats to induce skeletal muscle atrophy.","authors":"Samrita Mondal, Sukanya Srivastava, Swati Srivastava, Richa Rathor, Geetha Suryakumar","doi":"10.1007/s13105-025-01100-y","DOIUrl":"10.1007/s13105-025-01100-y","url":null,"abstract":"<p><p>Emerging research on microRNA has decoded its crucial role in gene regulation, development and diseases. Skeletal muscle atrophy is reported in several chronic diseases as well as prolonged stay at high altitude. miR-320-3p is reported to be upregulated in various chronic diseases including cancer, heart diseases, diabetes, and chronic kidney diseases. The present study evaluates the role of miR-320-3p expression in regulating apelin and its downstream signaling under hypobaric hypoxia (HH) at high altitude. The expression of miR-320-3p was found to be upregulated during 7days HH (7DHH) exposure at 25,000 ft as compared to control group. The targets for miR-320-3p were retrieved from miRWalk 3.0, TargetScan 8.0, miRTarBase 10.0 databases in Rattus norvegicus. Using in silico approach, 26 myokines were screened out of total 14,435 targets of rno-miR-320-3p and levels of few myokines were experimentally validated. The expression of apelin, decorin, osteocrin, meteorin-like myokines were found to be significantly decreased while myostatin was significantly increased during HH exposure as compared to control rats. Enhanced expression of Tgfb and p-Smad3 under 7DHH indicated activation of protein degradation pathways. Expression of Pgc1a and Nrf2, the critical regulators of mitochondrial biogenesis, were significantly decreased under HH. Thus, increased expression of miR-320-3p regulate apelin and modulate downstream signaling via attenuation of mitochondrial biogenesis and myogenesis. Hence, miR-320-3p and myokines play pivotal role to regulate skeletal muscle atrophy. Further research on potential targets of miR-320-3p regulating the muscle mass may lead to the development of novel therapeutics in personalized medicine to combat skeletal muscle diseases.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"751-770"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Postnatal overfeeding induces gut microbiota disturbances and impairs GPR43/FIAF/LPL pathway in the rat model of PCOS.","authors":"Nataša Veličković, Miloš Vratarić, Bojana Mićić, Ana Teofilović, Marina Radovanović, Sofija Ignjatović, Uroš Gašić, Ana Djordjevic, Djuro Macut, Danijela Vojnović Milutinović","doi":"10.1007/s13105-025-01103-9","DOIUrl":"10.1007/s13105-025-01103-9","url":null,"abstract":"<p><p>Women with polycystic ovary syndrome (PCOS) has high incidence of metabolic dysfunction-associated steatotic liver disease (MASLD). The development of PCOS-associated MASLD is accelerated by prepubertal obesity, therefore, we analyzed the impact of postnatal overfeeding-induced obesity on the gut microbiota and hepatic lipid metabolism in the PCOS rat model. Wistar rats were divided into 4 groups, where treatment with 5α-dihydrotestosterone (5α-DHT) stimulated hyperandrogenemia (DHT groups), whereas litter size reduction induced early postnatal overfeeding and obesity (SL groups). The fecal microbiota composition and diversity was analyzed by 16S rRNA sequencing. The bacterial metabolites level was measured by mass spectrometry. Hematoxylin-eosin staining, Western blots, and qRT-PCR were used to analyze hepatic lipid metabolism. Our results show that postnatal overfeeding shifted the microbiota composition towards obesity-associated genera, while hyperandrogenemia led to reduced β-diversity and increased abundance of androgen-regulated genera. Interaction of treatments reduced α- and β-diversity and decreased the abundance of beneficial butyrate-producing genera Roseburia, Oscillospira, and Ruminococcus and butyric acid plasma level. Shift in microbiota composition and activity was accompanied by decreased expression of G-protein coupled receptor (GPR) 43, fasting-induced adipocyte factor (FIAF) and increased expression of lipoprotein lipase (LPL). In accordance with altered GPR43 and FIAF/LPL pathway, increased expression of lipogenic transcription factors was observed in SL-DHT animals, but this did not result in hepatic lipid deposition. Our results demonstrated that postnatal overfeeding contributes to decreased richness and changes in gut microbiota composition in the PCOS animal model that is associated with impaired hepatic lipid metabolism, which may accelerate development of MASLD.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"793-813"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144553826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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 UCP1-independent thermogenesis: the role of futile cycles in energy dissipation.","authors":"Quanhao Sun, Xinyue Cui, Dong Yin, Juan Li, Jiarui Li, Likun Du","doi":"10.1007/s13105-025-01090-x","DOIUrl":"10.1007/s13105-025-01090-x","url":null,"abstract":"<p><p>Adipose tissue thermogenesis has emerged as a prominent research focus for the treatment of metabolic diseases, particularly through mitochondrial uncoupling, which oxidizes nutrients to produce heat rather than synthesizing ATP. Uncoupling protein 1 (UCP1) has garnered significant attention as a core protein mediating non-shivering thermogenesis(NST). However, recent studies indicate that energy dissipation can also occur via UCP1-independent thermogenesis, partially driven by futile metabolic cycles. These cycles involve ATP depletion coupled with reversible energy reactions, resulting in futile energy expenditure. Unlike classical UCP1-mediated thermogenesis, futile cycling is not confined to brown and beige adipose tissue, suggesting a broader range of therapeutic targets. These findings open new avenues for targeting these pathways to enhance metabolic health. This review explores the characteristics and distinctions of the primary metabolic organs (adipose tissue, liver, and skeletal muscle) involved in the futile cycles of thermogenesis. It further elaborates on the cellular and molecular mechanisms underlying calcium, creatine, and lipid cycling, emphasizing their strengths, limitations, and roles beyond thermogenesis.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"521-537"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Expression landscape of epigenetic genes in human hepatocellular carcinoma.","authors":"Borja Castelló-Uribe, Amaya López-Pascual, Jasmin Elurbide, Elena Adán-Villaescusa, Emiliana Valbuena-Goiricelaya, Luz A Martinez-Perez, Iker Uriarte, M Ujúe Latasa, Bruno Sangro, María Arechederra, Carmen Berasain, Matías A Avila, Maite G Fernández-Barrena","doi":"10.1007/s13105-025-01095-6","DOIUrl":"10.1007/s13105-025-01095-6","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is the most common primary liver tumor, often arising in the context of chronic liver disease. Despite recent advances in systemic therapies, including the use of immune checkpoint inhibitors (ICIs), clinical outcomes remain suboptimal, with many patients exhibiting primary or acquired resistance. Accumulating evidence indicates that the dysregulation of epigenetic mechanisms contributes to HCC development, and may also play a crucial role in shaping the tumor immune microenvironment, influencing responses to treatments. In this study, we analyzed the expression profiles of a comprehensive set of epigenetic regulators across publicly available transcriptomic datasets of HCC and non-tumoral liver tissues. Our findings reveal a consistent dysregulation of key epigenetic modifiers, particularly those involved in DNA methylation and histone modification. Furthermore, our analysis underscores the need for a deeper understanding of the epigenetic landscape of HCC, as specific epigenetic patterns are directly associated with disease development, the major mutational, immune, and transcriptional subclasses of HCC, and patient clinical outcomes. Our study provides a foundation for integrating epigenetic biomarkers into patient stratification and therapeutic decision-making. A more comprehensive analysis of epigenetic alterations could pave the way for novel predictive markers and combination strategies that could enhance the efficacy of ICIs in HCC.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"699-727"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373563/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144275177","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":"Correction: Acute pancreatitis experimental models, advantages and disadvantages.","authors":"Genaro J Rosales-Muñoz, Verónica Souza-Arroyo, Leticia Bucio-Ortiz, Roxana U Miranda-Labra, Luis E Gomez-Quiroz, María Concepción Gutiérrez-Ruiz","doi":"10.1007/s13105-025-01102-w","DOIUrl":"10.1007/s13105-025-01102-w","url":null,"abstract":"","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"831-832"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144317180","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 use of circulating miRNAs for the diagnosis, prognosis, and personalized treatment of MASLD.","authors":"Ana Luz Tobaruela-Resola, Fermín I Milagro, Paola Mogna-Pelaez, María Jesús Moreno-Aliaga, Itziar Abete, María Ángeles Zulet","doi":"10.1007/s13105-025-01110-w","DOIUrl":"10.1007/s13105-025-01110-w","url":null,"abstract":"<p><strong>Introduction: </strong>Metabolic dysfunction-associated steatotic liver disease (MASLD), formerly NAFLD, includes a range of conditions from steatosis to hepatocellular carcinoma and poses a significant health and economic burden. Circulating microRNAs (miRNAs) are key regulators of metabolic and inflammatory pathways involved in MASLD. However, their clinical utility as non-invasive biomarkers remain unclear. This review aims to clarify their diagnostic, prognostic, and therapeutic potential, addressing current gaps in the literature.</p><p><strong>Methods: </strong>Following PRISMA guidelines, we conducted a systematic review of 1149 studies from the PubMed and Scopus databases up to 2024, focused on circulating miRNAs in MASLD.</p><p><strong>Results: </strong>The most frequently studied miRNAs included miR-122 (35.56% of studies), miR-21 (18.89%), miR-34 (14.44%), and miR-192-5p (13.33%). Diagnostic accuracy varied among miRNAs, with miR-200 and miR-298 demonstrating AUROCs of 0.96 and 0.98, respectively, for MASLD detection. In MASH, miR-200, miR-298, and miR-342 exhibited near-perfect AUROCs of 0.99, while miR-122 showed values between 0.81 and 1.0. For HCC, miR-214 achieved an AUROC of 0.88, and miR-34a ranged from 0.73 to 0.76. Several miRNA panels demonstrated high diagnostic accuracy, with AUROCs up to 0.99, particularly in distinguishing HCC from other liver conditions. Prognostically, elevated miR-122 levels correlated with disease severity and fibrosis progression, while miR-21 and miR-223 were linked to obesity-associated MASH. Therapeutic interventions, including surgery, dietary modifications, and supplementation, were found to modulate miRNA profiles.</p><p><strong>Conclusions: </strong>MiRNAs exhibit strong potential as minimally invasive biomarkers for MASLD, contributing to improved diagnosis, prognosis, and therapeutic decision-making. Their stability and role in personalized medicine underscore their clinical relevance.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":" ","pages":"589-609"},"PeriodicalIF":4.3,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12373555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642766","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}