Cell Cycle最新文献_第8页

Meta-analysis of NPC2-mediated cholesterol transport in human cancers as a prognostic biomarker with therapeutic implications. npc2介导的胆固醇转运在人类癌症中作为具有治疗意义的预后生物标志物的meta分析。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2026-12-01 Epub Date: 2026-09-23 DOI: 10.1080/15384101.2026.2731645

Francisco Cezar Aquino de Moraes, Luis Henrique Rios Moreira Rego, Emanuele Rocha da Silva, Rosario Dominguez Crespo Hirata, Rommel Mario Rodriguez Burbano, Mario Hiroyuki Hirata

{"title":"Meta-analysis of NPC2-mediated cholesterol transport in human cancers as a prognostic biomarker with therapeutic implications.","authors":"Francisco Cezar Aquino de Moraes, Luis Henrique Rios Moreira Rego, Emanuele Rocha da Silva, Rosario Dominguez Crespo Hirata, Rommel Mario Rodriguez Burbano, Mario Hiroyuki Hirata","doi":"10.1080/15384101.2026.2731645","DOIUrl":"10.1080/15384101.2026.2731645","url":null,"abstract":"NPC2 is a lysosomal cholesterol transporter involved in intracellular lipid trafficking and cholesterol homeostasis, processes that have been increasingly implicated in cancer biology. To quantify the clinical impact of NPC2 expression across human malignancies, we analyzed survival data from 2,097 patients evaluated for NPC2 expression in tumor tissues. We conducted a random-effects meta-analysis of four eligible studies assessing NPC2 expression by mRNA (RNA-seq, qRT-PCR) and protein-based methods (immunohistochemistry, Western blot).The cohort included 756 patients with gastric cancer (36.0%), 374 with hepatocellular carcinoma (17.8%), and 967 with gliomas (46.2%). Pooled analyses demonstrated that elevated NPC2 expression was significantly associated with worse overall survival across cancers (HR 1.29, 95% CI 1.10-1.52, p = 0.001; I2 = 56%). In gastric cancer, this association was stronger and highly consistent (HR 1.37, 95% CI 1.18-1.60, p < 0.001; I2 = 0%). These results suggest that NPC2 overexpression identifies a subset of tumors with increased aggressiveness and adverse clinical outcomes. Collectively, these findings support NPC2 as a candidate adverse prognostic biomarker and highlight lysosomal cholesterol trafficking as a pathway of translational interest in cancer biology. Further mechanistic and clinical studies are warranted to clarify the biological role of NPC2 and its potential therapeutic implications.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":"25 1","pages":"1-12"},"PeriodicalIF":3.9,"publicationDate":"2026-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13613889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023978","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}

引用次数: 0

The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights. GABBR1/miR-19b-3p/WNT2B轴调节病毒感染糖尿病的胰岛素抵抗和肝损伤：机制和治疗见解

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-09-25 DOI: 10.1080/15384101.2025.2564744

Rui Yang, Jiangling Zhu, Lin Zou, Yingxuan Li, Li Peng, Xing Wang, Qian Xi, Fei Sun, Junhua Ma, Xia Chen

{"title":"The GABBR1/miR-19b-3p/WNT2B axis regulates insulin resistance and liver injury in diabetes with viral infection: mechanistic and therapeutic insights.","authors":"Rui Yang, Jiangling Zhu, Lin Zou, Yingxuan Li, Li Peng, Xing Wang, Qian Xi, Fei Sun, Junhua Ma, Xia Chen","doi":"10.1080/15384101.2025.2564744","DOIUrl":"10.1080/15384101.2025.2564744","url":null,"abstract":"Insulin resistance (IR) is the main feature of type 2 diabetes mellitus. Furthermore, viral infection can aggravate the abnormal glucose metabolism in diabetic patients. GABBR1 can maintain normal glucose homeostasis, but its specific role in diabetes is not clear. We investigated the function of the GABBR1/miR-19b-3p/WNT2B axis in vitro and in vivo. miR-19b-3p and GABBR1 were overexpressed or knocked down in AML12 cells. Subsequently, these cells were treated with palmitic acid (PA) to induce damage or poly I : C to mimic viral infection. The degree of AML12 cell damage was assessed using the CCK-8 assay; inflammation levels were measured using ELISA; and IR indexes were determined using the Immunofluorescence kit and Western blot assay. The diabetic mice model was established to evaluate liver injury and IR. PA and poly I : C can reduce the activity of AML12 cells, increase apoptosis and inflammatory factor contents, weaken the ability of glucose uptake and consumption, enhance the production capacity, and reduce the level of GLUT4. GABBR1 mediates the targeted regulation of WNT2B by miR-19b-3p. PA and poly I : C also increased ALT, AST, inflammatory factors and miR-19b-3p levels, and decreased GABBR1 and WNT2B expression of mice. Liver cells showed swelling and many spherical lipid droplets. After miR-19b-3p knockdown and GABBR1 overexpression, the degree of liver injury and IR in AML12 cells and mice were alleviated. GABBR1 regulates miR-19b-3p/WNT2B axis to reduce liver injury, IR and inflammatory response, and improve the comorbidity of diabetes and viral infection. This pathway represents a potential therapeutic target for mitigating the comorbidity of diabetes and viral infection.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"566-585"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918276/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147837","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}

引用次数: 0

Enigmatic functions of ATP8B1: cholestasis, inflammation, phosphoinositide flipping, and cellular homeostasis. ATP8B1的神秘功能：胆汁淤积、炎症、磷酸肌肽翻转和细胞内稳态。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-14 DOI: 10.1080/15384101.2025.2574275

Ashutosh Prince, C Alicia Traughber, Yavar Shiravand, Nilam Bhandari, Mariam R Khan, Swati Sharma, Kara Timinski, Karen F Murray, Laura N Bull, Kailash Gulshan

{"title":"Enigmatic functions of ATP8B1: cholestasis, inflammation, phosphoinositide flipping, and cellular homeostasis.","authors":"Ashutosh Prince, C Alicia Traughber, Yavar Shiravand, Nilam Bhandari, Mariam R Khan, Swati Sharma, Kara Timinski, Karen F Murray, Laura N Bull, Kailash Gulshan","doi":"10.1080/15384101.2025.2574275","DOIUrl":"10.1080/15384101.2025.2574275","url":null,"abstract":"Mutations in ATP8B1 cause a spectrum of cholestatic liver disease, ranging from Progressive-Familial-Intrahepatic-Cholestasis type-1 (PFIC1) to Benign-Recurrent-Intrahepatic-Cholestasis type-1 (BRIC1). Manifestations of PFIC1 include severe pruritus, jaundice, and liver damage. Extrahepatic features sometimes observed in PFIC1 include sensorineural hearing loss, diarrhea, pancreatitis, and short stature. ATP8B1 was shown to translocate phospholipids across the plasma membrane; however, expression of ATP8B1 in many tissues and the range of pathological manifestations in ATP8B1 deficiency suggest diverse physiological functions of ATP8B1, and pleiotropic mechanisms regulating its activity. Recent studies suggest that phosphoinositides, including PIP2 and PIP3, can function as regulators, substrates, and binding partners of ATP8B1. New research shows that ATP8B1 modulates host immune system by regulating cleavage of pyroptotic-executioner Gasdermin D (GSDMD), and inflammation-resolution pathways such as phagocytosis/efferocytosis. Further mechanistic insights can accelerate development of new therapies for restoring membrane integrity, reducing inflammasome activity, and correcting metabolic imbalances caused by ATP8B1 dysfunction.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"409-421"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918318/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145285728","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}

引用次数: 0

Advances in DNA damage repair mechanisms in stem cells and their applications. 干细胞DNA损伤修复机制及其应用研究进展。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-24 DOI: 10.1080/15384101.2025.2576514

Dongxu Wei, Yuhao Chang, Yao Yang, Xuanbai Chen, Shiqi Jin, Kainan Huang, Zeyidan Jiapaer, Xianli Wang

引用次数: 0

HSP22 reduces diabetic cardiomyopathy by inhibition oxidative stress and inflammation. HSP22通过抑制氧化应激和炎症降低糖尿病性心肌病。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-04 DOI: 10.1080/15384101.2025.2581629

Lingling Yu, Shengsong Chen, Weifang Zhang, Chahua Huang, Longlong Hu, Liang Liu, Yun Yu, Qian Liang, Huihui Bao, Xiaoshu Cheng

{"title":"HSP22 reduces diabetic cardiomyopathy by inhibition oxidative stress and inflammation.","authors":"Lingling Yu, Shengsong Chen, Weifang Zhang, Chahua Huang, Longlong Hu, Liang Liu, Yun Yu, Qian Liang, Huihui Bao, Xiaoshu Cheng","doi":"10.1080/15384101.2025.2581629","DOIUrl":"10.1080/15384101.2025.2581629","url":null,"abstract":"Heat shock protein 22 (HSP22) can reduce type 2 diabetes mellitus (T2DM) induced vascular endothelial injury by inhibition of inflammation and oxidative stress. Therefore, we explored whether HSP22 alleviated diabetes cardiomyopathy (DCM) in mice. A T2DM mouse model was constructed and myocardial tissues were used to perform transcriptome sequencing. HSP22 transgenic and HSP22 knockout mice were established to confirm its role in DCM. Transthoracic echocardiography, hematoxylin-eosin staining, TUNEL staining and apoptosis-related proteins were detected to evaluate myocardial injury. Dihydroethidium staining, malondialdehyde and superoxide dismutase levels were detected to evaluate myocardial oxidative stress. We performed RT-PCR to detect inflammatory factors and evaluate the myocardial inflammatory response. Immunohistochemical staining, RT-PCR and western blot were used to define the expression of HSP22 in mouse myocardial tissues. Transcriptome sequencing analysis revealed the expression of HSP22 in myocardium of T2DM mice significantly decreases. GO analysis found that oxidative stress and inflammatory response were closely related to DCM in mice. Furthermore, HSP22 overexpression can alleviate DCM in mice and HSP22 knockout aggravated DCM. HSP22 reduced oxidative stress and inflammation to alleviate DCM in mice.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"655-669"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918273/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145437481","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}

引用次数: 0

Exosomes in hepatocellular carcinoma: involvement in reprogramming the tumor microenvironment for immune evasion, metastasis, angiogenesis, and drug resistance. 肝细胞癌中的外泌体：参与肿瘤微环境的重编程，以促进免疫逃避、转移、血管生成和耐药性。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-08 DOI: 10.1080/15384101.2025.2583289

Mahsa Ghasemian-Irani, Shabnam Babaei, Tohid Kazemi

{"title":"Exosomes in hepatocellular carcinoma: involvement in reprogramming the tumor microenvironment for immune evasion, metastasis, angiogenesis, and drug resistance.","authors":"Mahsa Ghasemian-Irani, Shabnam Babaei, Tohid Kazemi","doi":"10.1080/15384101.2025.2583289","DOIUrl":"10.1080/15384101.2025.2583289","url":null,"abstract":"Hepatocellular carcinoma (HCC) is a highly aggressive liver cancer, and its progression is significantly influenced by the tumor microenvironment (TME). Tumor-derived exosomes (TEXs), an important component of the TME, significantly influence tumor growth by regulating immune responses, facilitating metastasis, and enhancing resistance to therapy. These extracellular vesicles (EVs) transport bioactive substances, such as proteins, lipids, and nucleic acids that promote interaction between cells in the TME. Recent research indicates that HCC-derived exosomes can inhibit immune cell activity, specifically in T cells, thus creating an immunosuppressive TME that facilitates tumor immune escape. They also augment metastatic capability by restructuring the extracellular matrix and promoting angiogenesis. Moreover, HCC-derived exosomes have been associated with developing resistance to drug therapy by transferring molecules such as apoptotic signals and oncogenic microRNAs, circRNAs and lncRNA. Understanding how HCC-derived exosomes affect immune modulation, metastasis, and drug resistance could yield innovative therapeutic targets to enhance therapy outcomes. This review focuses on recent research on the diverse functions of TEXs in HCC progression.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"529-551"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918322/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145470676","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}

引用次数: 0

Epithelial-mesenchymal-associated non-coding RNAs as Breast cancer metastasis biomarkers. 上皮-间质相关非编码rna作为乳腺癌转移的生物标志物。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-18 DOI: 10.1080/15384101.2025.2576512

Nika Asefi, Ahmad Fazilat, Tayebe Oghabi, Narges Jafarbeik Iravani, Keivan Majidzadeh-A, Farkhonde Hasannejad

{"title":"Epithelial-mesenchymal-associated non-coding RNAs as Breast cancer metastasis biomarkers.","authors":"Nika Asefi, Ahmad Fazilat, Tayebe Oghabi, Narges Jafarbeik Iravani, Keivan Majidzadeh-A, Farkhonde Hasannejad","doi":"10.1080/15384101.2025.2576512","DOIUrl":"10.1080/15384101.2025.2576512","url":null,"abstract":"Breast cancer (BC) is identified as a significant cause of cancer mortality in the female population. The recurrence of initial tumors and the metastasis to remote areas of the body are significant factors leading to the mortality linked with BC. Despite the advancements in diagnostic and therapeutic approaches, a comprehensive understanding of the molecular mechanisms underlying metastasis is still unclear, particularly regarding the regulatory role of non-coding RNAs (ncRNAs) in epithelial-mesenchymal transition (EMT). Different categories of ncRNAs, including microRNAs (miRNAs), circular RNAs (circRNAs), and long ncRNAs (lncRNAs), can manage the complex regulatory frameworks of EMT at various levels. Since dysregulation of ncRNAs is associated with key processes in EMT, investigating them as valuable tools for identifying the metastatic potential of tumors at an early stage could significantly increase diagnostic accuracy and improve patient outcomes, particularly in BC. This review aims to bridge this gap by systematically summarizing current insights into the interplay between EMT and various classes of ncRNAs in the context of BC progression. We discuss the molecular pathways through which ncRNAs regulate EMT, their impact on metastasis and explore their potential as diagnostic biomarkers and therapeutic targets. By providing an integrative overview of recent findings, this article highlights unresolved questions and proposes directions for future research, offering a valuable resource for researchers and clinicians involved in breast cancer biology and treatment development.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"440-467"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710946/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145312427","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}

引用次数: 0

The curvature code: BCL-w dimers rewire BAX-BCL-2 control of mitochondrial fate and apoptosis. 曲率代码：BCL-w二聚体重新连接BAX-BCL-2对线粒体命运和凋亡的控制。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-12-01 DOI: 10.1080/15384101.2025.2597275

Gaetano Santulli

引用次数: 0

The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification. 甲基转移酶METTL3通过调节EGF m6A修饰促进乳腺癌细胞的进展。

IF 3.9 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-10-08 DOI: 10.1080/15384101.2025.2570258

Jiaqing Liu, Han Fang, Xinhao Yang, Yi Lu, Enjie Li, Meina Wang, Zhigang Hu

{"title":"The methyltransferase METTL3 promotes the progression of breast cancer cells via regulating EGF m6A modification.","authors":"Jiaqing Liu, Han Fang, Xinhao Yang, Yi Lu, Enjie Li, Meina Wang, Zhigang Hu","doi":"10.1080/15384101.2025.2570258","DOIUrl":"10.1080/15384101.2025.2570258","url":null,"abstract":"Ranking second out of new cancer cases, breast cancer (BRCA) is the leading cause of cancerous death among women globally. Methyltransferase-like 3 (METTL3), as the well-known N6‑methyladenosine (m6A) \"writer\" with catalytic function, regulates cancer progression through specific downstream targets, but its interplay with epidermal growth factor (EGF) signaling in BRCA is poorly defined. Here, we depict a METTL3-m6A-EGF axis in BRCA, where BRCA cell properties were affected by METTL3 through m6A-dependent expression of EGF. We observed the correlation between METTL3 expression in BRCA tissues and negative prognosis through bioinformatics analysis and RT-qPCR. In vitro lentiviral-mediated METTL3 knockdown suppressed proliferation and migration, while the in vivo tumor formation experiment in nude mice validated the tumor-promoting effect of METTL3. Hematoxylin-eosin staining and immunohistochemistry also showed the tumor-promoting effect of METTL3. Mechanistically, METTL3 stabilized EGF mRNA via m6A modification, as evidenced by MeRIP-qPCR and Western blotting. Notably, METTL3 maintains EGF/EGFR signaling, and its overexpression leads to insensitivity to gefitinib and adriamycin. We naturally conclude that METTL3 is a central epigenetic regulator of EGF-driven BRCA progression, providing a rationale for targeting METTL3 to overcome chemotherapeutic resistance.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"605-618"},"PeriodicalIF":3.9,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12710917/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145250057","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}

引用次数: 0

"Leucine zipper proteins as emerging therapeutic regulators: structural dynamics, disease associations, and novel targeting strategies". 亮氨酸拉链蛋白作为新兴的治疗调节剂：结构动力学、疾病关联和新的靶向策略。

IF 3.4 3区生物学

Cell Cycle Pub Date : 2025-11-01 Epub Date: 2025-11-06 DOI: 10.1080/15384101.2025.2585073

Anjali Kumari, Adiba Mussarrat, Manodeep Chakraborty, Ananya Bhattacharjee, Ravi Kumar Rajan

{"title":"\"Leucine zipper proteins as emerging therapeutic regulators: structural dynamics, disease associations, and novel targeting strategies\".","authors":"Anjali Kumari, Adiba Mussarrat, Manodeep Chakraborty, Ananya Bhattacharjee, Ravi Kumar Rajan","doi":"10.1080/15384101.2025.2585073","DOIUrl":"10.1080/15384101.2025.2585073","url":null,"abstract":"Leucine zipper proteins are transcription factors that regulate gene activity through DNA binding and creating stable pairs. They are located in particular tissues and are involved in significant processes like metabolism, immunity, and stress response. The C/EBPβ (CCAAT/Enhancer-Binding Proteins), which is predominantly active in the liver and spleen, regulates metabolism and immune activity. The GILZ (glucocorticoid-induced leucine zipper), which is located in the brain, lungs, immune cells, and reproductive system, may protect against inflammation and stress. Hormonal signals or oxidative stress may cause these proteins to be activated and transported to the nucleus to turn off or turn on the genes. The disruption of balance, such as the loss of GILZ, drives inflammation, which may cause diseases. Therapies include small molecules, peptides, or DNA decoy therapy. The selective control of these proteins via biomarker profiling and targeted tissue delivery has potential in mitigating cancer, inflammatory, and metabolic diseases.","PeriodicalId":9686,"journal":{"name":"Cell Cycle","volume":" ","pages":"552-565"},"PeriodicalIF":3.4,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12918286/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145450780","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}

引用次数: 0