Cell Biology and Toxicology最新文献

{"title":"A novel SIRT1 activator attenuates neuropathic pain by inhibiting spinal neuronal activation via the SIRT1-mGluR1/5 pathway.","authors":"Xiaobao Ding, Guizhi Wang, Yuwen Lin, Wenli Hu, Chen Chen, Jian Gao, Yuqing Wu, Chenghua Zhou","doi":"10.1007/s10565-024-09970-6","DOIUrl":"10.1007/s10565-024-09970-6","url":null,"abstract":"<p><p>Neuropathic pain is a type of pain caused by an injury or disease of the somatosensory nervous system. Currently, there is still absence of effective therapeutic drugs for neuropathic pain, so developing new therapeutic drugs is urgently needed. In the present study, we observed the effect of Comp 6d, a novel silent information regulator 1 (SIRT1) activator synthesized in our laboratory, on neuropathic pain and investigated the mechanisms involved. We found that both intrathecal and intraperitoneal injections of Comp 6d effectively alleviated neuropathic pain induced by chronic constriction injury (CCI) or spared nerve injury (SNI). However, the effect of Comp 6d on neuropathic pain was abolished in SIRT1 knockout mice. These results demonstrated that Comp 6d alleviated neuropathic pain by specifically activating SIRT1 in the spinal cord. Moreover, long-term intraperitoneal injection of Comp 6d had no significant side effects on heart, liver and kidney in SNI mice. Further study showed that the improvement of neuropathic pain by Comp 6d was mediated by the downregulation of mGluR1/5 levels and the subsequent inhibition of spinal neuronal activation. Taken together, the present findings suggest that the novel SIRT1 activator Comp 6d inhibits the activation of spinal cord neurons via the SIRT1-mGluR1/5 pathway, thereby attenuating neuropathic pain. Comp 6d is expected to be an effective therapeutic agent for neuropathic pain.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"24"},"PeriodicalIF":5.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11711878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Exosomal NEDD4L derived from HG+oxLDL-induced vascular endothelial cells accelerates macrophage M1 polarization and oxLDL uptake by ubiquitinating IκBα and PPARγ.","authors":"Guozhu Chen, Yisong Pei, Peng Jiang, Qiaoling Ye, Zulong Xie, Laxman Gyawali","doi":"10.1007/s10565-024-09973-3","DOIUrl":"10.1007/s10565-024-09973-3","url":null,"abstract":"<p><strong>Background: </strong>Vascular endothelial cell-derived exosomes are thought to mediate disease progression by regulating macrophage polarization. However, its mechanism in diabetes mellitus (DM)-related atherosclerosis (AS) progress is unclear.</p><p><strong>Methods: </strong>High-glucose (HG) and oxLDL were used to induce human cardiac microvascular endothelial cells (HCMECs) to mimic DM-related AS model. The conditioned medium (CM) from HG+oxLDL-induced HCMECs was incubated with THP1-M0 monocytes treated with LPS or oxLDL. The mRNA levels of macrophage M1/M2 polarization markers, NEDD4L, IκBα and PPARγ were determined by qRT-PCR. Flow cytometry was used to analyze macrophage marker. Dil-labeled oxLDL and oil red O staining were performed to assess oxLDL uptake by THP1-M0 cells. The levels of inflammatory factors were examined using ELISA. Transmission electron microscope was used for observing foam cell formation and exosome morphology. The protein levels of p-Smad1/Smad1, p-Smad2/Smad2, p-IκBα/IκBα, p-P65/P65, anti-lipid metabolism-related markers, and NEDD4L were tested by western blot. The interaction between NEDD4L and IκBα or PPARγ was assessed by Co-IP assay.</p><p><strong>Results: </strong>The CM of HG+oxLDL-induced HCMECs could promote macrophage M1 polarization, oxLDL uptake and foam cell formation, and exosome inhibiter GW4869 eliminated these effects. NEDD4L was overexpressed in exosomes from HG+oxLDL-induced HCMECs, which could be taken up by THP1-M0 cells. Exosomal NEDD4L knockdown inhibited macrophage M1 polarization, oxLDL uptake and foam cell formation by reducing the protein levels of p-Smad1/Smad1, p-Smad2/Smad2, p-IκBα/IκBα and p-P65/P65. NEDD4L could reduce IκBα and PPARγ expression through ubiquitination.</p><p><strong>Conclusion: </strong>HG+oxLDL-induced HCMECs-derived exosomal NEDD4L could enhance the ubiquitination of IκBα and PPARγ to facilitate macrophage M1 polarization and oxLDL uptake, thus accelerating DM-related AS.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"23"},"PeriodicalIF":5.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11706887/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142945293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF112, whose transcription is regulated by KLF4, inhibits colorectal cancer growth via promoting ubiquitin-dependent degradation of NAA40.","authors":"Chunfei Li, Wenzheng Guan, Donghua Geng, Yong Feng","doi":"10.1007/s10565-024-09977-z","DOIUrl":"10.1007/s10565-024-09977-z","url":null,"abstract":"<p><strong>Background: </strong>RING finger protein 112 (RNF112) exerts a key role in human tumors. However, its biological function in colorectal cancer (CRC) has not been discussed. We aimed to explore the function and molecular mechanism of RNF112 in CRC.</p><p><strong>Results: </strong>In this study, RNF112 expression was notably decreased in CRC tissues and cells. Clinical analysis revealed a significant association between low RNF112 expression and tumor size, N classification and TNM stage. In vitro experiments demonstrated that overexpression of RNF112 repressed cell viability, promoted cell cycle arrest and apoptosis, while knocking down RNF112 had the opposite function. The tumor formation results in nude mice supported that RNF112 overexpression exerted anti-tumor effects by inhibiting cell growth and promoting cell apoptosis. Mechanistically, Krüppel-like factor 4 (KLF4) acted as an upstream regulator of RNF112 by mediating its transcription. Furthermore, we explored the downstream mechanism of RNF112 and discovered that it promoted ubiquitination and degradation of oncoprotein N-alpha-acetyltransferase 40 (NAA40) through ubiquitin ligase activity. In addition, overexpression of NAA40 eliminated the effect of RNF112 overexpression on CRC tumorigenesis.</p><p><strong>Conclusions: </strong>In summary, our findings confirm that RNF112, whose transcription is regulated by KLF4, inhibits CRC growth through promoting ubiquitin-dependent degradation of NAA40. We have unraveled the mechanism of KLF4-RNF112-NAA40 axis in CRC, which shed light on the therapeutic strategies for this disease.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"22"},"PeriodicalIF":5.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11700914/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142930773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of cancer-associated fibroblast subtypes and prognostic model development in breast cancer: role of the RUNX1/SDC1 axis in promoting invasion and metastasis.","authors":"Yunhao Wu, Nu Li, Jin Shang, Jiazi Jiang, Xiaoliang Liu","doi":"10.1007/s10565-024-09950-w","DOIUrl":"10.1007/s10565-024-09950-w","url":null,"abstract":"<p><p>In this study, we identified cancer-associated fibroblast (CAF) molecular subtypes and developed a CAF-based prognostic model for breast cancer (BRCA). The heterogeneity of cancer-associated fibroblasts (CAFs) and their significant involvement in the advancement of BRCA were discovered employing single-cell RNA sequencing. Notably, we discovered that the RUNX1/SDC1 axis enhances BRCA cell invasion and metastasis. RUNX1 transcriptionally upregulates SDC1, which facilitates extracellular matrix remodeling and promotes tumor cell migration. This finding highlights the vital contribution of CAFs to the tumor microenvironment and provides new potential targets for therapeutic intervention. The predictive model showcased remarkable precision in anticipating patient outcomes and could guide personalized treatment strategies.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"21"},"PeriodicalIF":5.3,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11698906/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142926788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNAJB4/HLJ1 deficiency sensitizes diethylnitrosamine-induced hepatocarcinogenesis with peritumoral STAT3 activation.","authors":"Wei-Jia Luo, Wei-Lun Hsu, Chih-Yun Lu, Min-Hui Chien, Jung-Hsuan Chang, Kang-Yi Su","doi":"10.1007/s10565-024-09978-y","DOIUrl":"10.1007/s10565-024-09978-y","url":null,"abstract":"<p><p>Environmental chemicals and toxins are known to impact human health and contribute to cancer developments. Among these, genotoxins induce genetic mutations critical for cancer initiation. In the liver, proliferation serves not only as a compensatory mechanism for tissue repair but also as a potential risk factor for the progression of premalignant lesions. The role of Human Liver DnaJ-Like Protein (DNAJB4/HLJ1), a stress-responsive heat shock protein 40, in genotoxin-induced liver carcinogenesis remains unexplored. Using whole-genome transcriptomic analysis, we demonstrate that HLJ1 deficiency in mice results in altered gene signatures enriched in pathways associated with chemically induced liver cancer and IL-6/STAT3 signaling activation. Employing diethylnitrosamine (DEN) as a carcinogen, we further reveal that STAT3 and H2AX phosphorylation induced by short-term DEN treatment are amplified in HLJ1-deficient mice. In long-term DEN experiments, HLJ1 deletion enhances tumor proliferation and progression, accompanied by pronounced STAT3 phosphorylation in normal tissues rather than in tumor regions. The tumor-suppressive role of peritumoral HLJ1 is validated through the transplantation of HLJ1-wildtype B16F1 and LLC cancer cell lines into syngeneic HLJ1-deficient mice, which exhibits an augmented tumorigenic phenotype compared to wildtype controls. This study uncovers a previously unrecognized role of HLJ1 in suppressing liver carcinogenesis via the downregulation of STAT3 signaling in peritumoral normal cells. These findings suggest that HLJ1 reinforcement represents a promising strategy for liver cancer treatment and prevention.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"20"},"PeriodicalIF":5.3,"publicationDate":"2024-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11685265/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142909489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advances of NAT10 in diseases: insights from dual properties as protein and RNA acetyltransferase.","authors":"Bin Xiao, Shunhong Wu, Yan Tian, Weikai Huang, Guangzhan Chen, Dongxin Luo, Yishen Cai, Ming Chen, Yuqian Zhang, Chuyan Liu, Junxiu Zhao, Linhai Li","doi":"10.1007/s10565-024-09962-6","DOIUrl":"10.1007/s10565-024-09962-6","url":null,"abstract":"<p><p>N-acetyltransferase 10 (NAT10) is a member of the Gcn5-related N-acetyltransferase (GNAT) family and it plays a crucial role in various cellular processes, such as regulation of cell mitosis, post-DNA damage response, autophagy and apoptosis regulation, ribosome biogenesis, RNA modification, and other related pathways through its intrinsic protein acetyltransferase and RNA acetyltransferase activities. Moreover, NAT10 is closely associated with the pathogenesis of tumors, Hutchinson-Gilford progeria syndrome (HGPS), systemic lupus erythematosus, pulmonary fibrosis, depression and host-pathogen interactions. In recent years, mRNA acetylation has emerged as a prominent focus of research due to its pivotal role in regulating RNA stability and translation. NAT10 stands out as the sole identified modification enzyme responsible for RNA acetylation. There remains some ambiguity regarding the similarities and differences in NAT10's actions on protein and RNA substrates. While NAT10 involves acetylation modification in both cases, which is a crucial molecular mechanism in epigenetic regulation, there are significant disparities in the catalytic mechanisms, regulatory pathways, and biological processes involved. Therefore, this review aims to offer a comprehensive overview of NAT10 as a protein and RNA acetyltransferase, covering its basic catalytic features, biological functions, and roles in related diseases.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"17"},"PeriodicalIF":5.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"AP-1 activates KCNN4-mediated Ca2⁺ signaling to induce the Th1/Th17 differentiation of CD4⁺ cells in chronic non-bacterial prostatitis.","authors":"Jingfei Teng, Zhuomin Jia, Feng Gao, Yawei Guan, Li Yao, Chong Ma, Zhihui Li, Xing Ai","doi":"10.1007/s10565-024-09967-1","DOIUrl":"10.1007/s10565-024-09967-1","url":null,"abstract":"<p><p>The intraprostatic inflammatory infiltrate is characterized by Th1 CD4⁺ T cells, and its molecular mechanism is not well defined. This study explored the mechanisms responsible for the alteration of Th1/Th17 differentiation of CD4⁺ T cells in chronic non-bacterial prostatitis (CNP). CNP rats were induced by the administration of testosterone and 17β-estradiol. The Th1/Th17 cell percentage was increased in the prostate tissue of CNP rats, which was accompanied by increased IL-2, IFN-γ, IL-17A, and IL-22 levels. Transcriptome sequencing was performed, followed by KEGG pathway enrichment analysis. Activator protein-1 (AP-1) was enhanced in CD4⁺ T cells from CNP rats, and its inhibitor SR11302 suppressed Th1/Th17 differentiation and delayed CNP. AP-1 transcriptionally activated the expression of KCNN4, which potentiated mTORC1 in CD4⁺ T cells by enhancing Ca2⁺ signaling, thereby promoting Th1/Th17 differentiation. Rapamycin-mediated autophagy activation reversed AP-1/KCNN4/mTORC1-promoted Th1/Th17 differentiation, thereby inhibiting CNP. These results suggest that AP-1-mediated KCNN4 transcription promotes the inhibition of autophagy by mTORC1 through Ca2⁺ signaling, which supports Th1/Th17 differentiation of CD4⁺ T cells, resulting in the transformation of CNP to prostatic intraepithelial neoplasia and adenocarcinoma.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"18"},"PeriodicalIF":5.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680619/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RBM19 promotes the progression of prostate cancer under docetaxel treatment via SNHG21/PIM1 axis.","authors":"Wei Zhuang, Siwei Xu, Qingliu He, Qingfu Su, Heyi Chen, Jiabi Chen, Congming Huang, Zhijiao You","doi":"10.1007/s10565-024-09985-z","DOIUrl":"10.1007/s10565-024-09985-z","url":null,"abstract":"<p><p>RBM family proteins plays the critical role in the progression of numerous tumors. However, whether RBM family proteins involved in prostate cancer (PCa) progression is remain elucidated. In our study, an RNAi screen containing shRNA library targeting 54 members of the RBM family was applied to identify the critical RBM proteins involved in prostate cancer progression under docetaxel treatment, and RBM19 was selected. RBM19 was up-regulated in PCa specimens and correlated with the prognosis and Gleason score of PCa patients. Functionally assays revealed that RBM19 promoted PCa progression under docetaxel treatment both in vivo and in vitro. Mechanistically, RBM19 could bind to LncRNA SNHG21, thereby increased SNHG21 expression through enhancing its stability. Furthermore, SNHG21 bind to PIM1 proteins and prevented it from ubiquitin-protease dependent degradation and ultimately enhancing mitochondrial homeostasis. Overall, our study indicates the RBM19/SNHG21/PIM1 axis may be the encouraging target for docetaxel-tolerance PCa treatment.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"19"},"PeriodicalIF":5.3,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680647/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892400","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting CDK1 and copper homeostasis in breast cancer via a nanopolymer drug delivery system.","authors":"Nan Shang, Lisi Zhu, Yan Li, Chengyang Song, Xiaodan Liu","doi":"10.1007/s10565-024-09958-2","DOIUrl":"10.1007/s10565-024-09958-2","url":null,"abstract":"<p><p>The prevalence of breast cancer (BRCA) is notable in the female population, being a commonly diagnosed malignancy, where the management of copper levels is crucial for treatment success. This research aims to explore the influence of copper homeostasis on BRCA therapy, with a specific focus on the role of Cyclin-Dependent Kinase 1 (CDK1) and its relationship to copper regulation. A novel thermosensitive hydrogel incorporating nanoparticles (NPs) was engineered to synergize with the chemotherapy drug vincristine (VCR) in inhibiting tumor growth and metastasis. Through a comprehensive approach involving bioinformatics analyses, in vitro experiments, and in vivo models, the study identified CDK1 as a significant factor in BRCA progression under copper homeostasis. MBVP-Gel, a novel thermosensitive hydrogel incorporating NPs, was developed to enhance the delivery of chemotherapy drugs and regulate copper homeostasis in breast cancer treatment. The MBVP-Gel, formulated with copper chelation and VCR NPs, effectively suppressed CDK1 expression, thereby restraining BRCA cell growth and metastasis while enhancing the therapeutic impact of VCR. This investigation offers fresh insights and experimental validation on the interaction between copper homeostasis and BRCA, providing a valuable foundation for refining future treatment strategies. These findings underscore the potential advantages of targeting copper homeostasis and CDK1 in enhancing BRCA therapy, setting the stage for individualized interventions and improved patient consequences.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"16"},"PeriodicalIF":5.3,"publicationDate":"2024-12-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11671568/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892401","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HMGA1 influence on iron-induced cell death in Tfh cells of SLE patients.","authors":"Shan Zhao, Xiaotong Chen, Bohan Chang, Bailing Tian","doi":"10.1007/s10565-024-09955-5","DOIUrl":"10.1007/s10565-024-09955-5","url":null,"abstract":"<p><p>The autoimmune disorder known as Systemic Lupus Erythematosus (SLE) exhibits intricate features with abnormal immune responses leading to tissue injury. The generation of antibodies and the disruption of immune regulation heavily depend on the pivotal function of T follicular helper (Tfh) cells. Iron dysregulation is significant in autoimmune diseases, impacting immune cell function and disease progression. Our study investigates the role of the HMGA1/EZH2/STAT3/GPX4 axis in modulating Tfh cells and iron homeostasis in SLE. Abnormal Tfh cell populations in SLE patients demonstrate reduced susceptibility to iron-induced cell death, with HMGA1 identified as a key player in Tfh cell proliferation and sensitivity to iron-induced death. Experimental interventions reveal the inhibitory role of the HMGA1 axis in Tfh cells' susceptibility to iron-induced death, suggesting therapeutic avenues for SLE and related autoimmune disorders. Our study underscores the importance of iron homeostasis in autoimmune conditions, providing novel insights and treatment strategies for further research in this field.</p>","PeriodicalId":9672,"journal":{"name":"Cell Biology and Toxicology","volume":"41 1","pages":"6"},"PeriodicalIF":5.3,"publicationDate":"2024-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11662042/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}