Biochemical pharmacology最新文献

{"title":"Corrigendum to \"MNAM enhances Blautia abundance and modulates Th17/Treg balance to alleviate diabetes in T2DM Mice\" [Biochem. Pharmacol. volume (230), Part 2, Published online October 23, 2024/116593].","authors":"Jingfan Zhang, Yu Chen, Ling Li, Ruiqi Liu, Ping Li","doi":"10.1016/j.bcp.2024.116738","DOIUrl":"https://doi.org/10.1016/j.bcp.2024.116738","url":null,"abstract":"","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"116738"},"PeriodicalIF":5.3,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963667","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cordycepin alleviates metabolic dysfunction-associated liver disease by restoring mitochondrial homeostasis and reducing oxidative stress via Parkin-mediated mitophagy.","authors":"Hai-Ying Tian, Dao-Jiang Yu, Teng Xie, Meng-Xia Xu, Yu-Hao Wang, Xi-Lu Sun, Xin-Meng Zhou, Ying-Xuan Han, Qing-Qing Liao, Yu-Jie Zhao, Juan Liao, Mohamed El-Kassas, Xiao-Dong Sun, Yuan-Yuan Zhang","doi":"10.1016/j.bcp.2025.116750","DOIUrl":"10.1016/j.bcp.2025.116750","url":null,"abstract":"<p><p>The prevalence of metabolic dysfunction-associated steatotic liver disease (MASLD) keeps rising with only a few drugs available. The present study aims to investigate the effects and mechanisms of cordycepin on MASLD. Male C57BL/6 mice were induced with a 90-day high-fat diet (HFD) and intraperitoneal administration with streptozotocin to establish MASLD murine model. Then they were randomly divided into the HFD and cordycepin groups (15, 30, 45 mg/kg). Cordycepin was orally given for 30 days. Serum total cholesterol (TC), triacylglyceride (TG), and aspartate aminotransferase (AST) levels were measured. L02 cells were induced by oleate acid (OA) or lipopolysaccharides (LPS), and treated with cordycepin or combined with inhibitors including chloroquine, 3-Methyladenine, and compound C. Atg7 and Parkin were knocked down in L02 cells using siRNA. Oil Red O and Nile Red staining for measuring lipid deposition. Mitochondria were visualized by transfection with mCherry-TOMM20-N10. Quantitative real-time PCR, Western blotting, and immunofluorescence staining were used to determine expressions of key molecules in inflammation, lipid metabolism, mitochondria homeostasis, and oxidative stress. Cordycepin significantly mitigated lipid deposition and ballooning in the livers of MASLD mice. Serum TC, TG, and AST levels were decreased by cordycepin. Cordycepin alleviated OA-induced lipid deposition and LPS-induced inflammation in L02 cells, attenuated oxidative stress, promoted autophagy, and maintained the autophagic flux by activating AMP-activated protein kinase (AMPK). Cordycepin reduced the accumulation of impaired mitochondria by enhancing Parkin-dependent mitophagy and promoting mitochondrial biogenesis. Cordycepin alleviates MASLD by restoring mitochondrial homeostasis and reducing oxidative stress via activating the Parkin-mediated mitophagy.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116750"},"PeriodicalIF":5.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963682","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Guggulsterone ameliorates psoriasis by inhibiting keratinocyte proliferation and inflammation through induction of miR-17 directly targeting JAK1 and STAT3.","authors":"Lu Xiang, Yangli Shen, Shuangteng Liu, Bowen Fan, Jiafeng Zhan, Yadi Zhou, Baichun Jiang, Molin Wang, Qiao Liu, Xiaofei Liu, Yongxin Zou, Shuna Sun","doi":"10.1016/j.bcp.2025.116745","DOIUrl":"10.1016/j.bcp.2025.116745","url":null,"abstract":"<p><p>The pathogenesis of psoriasis involves hyperproliferation of epidermal keratinocytes and abnormal interactions between activated keratinocytes and infiltrating immune cells. Emerging evidence has shown that keratinocytes play essential roles in both the initiation and maintenance of psoriasis, suggesting that exposing keratinocytes to agents with antiproliferative and anti-inflammatory effects may be effective for psoriasis treatment. Guggulsterone (GS), a plant sterol derived from the gum resin of Commiphora wightii, possesses a variety of pharmacological activities. However, the effects of GS on psoriasis and the underlying mechanism have not been elucidated. In this study, we evaluated the therapeutic effect of GS on psoriasis using an imiquimod-induced psoriasis mouse model and investigated the effect of GS on human keratinocytes and the underlying mechanism. We found that GS effectively alleviated psoriasis-like skin lesions in imiquimod-induced psoriasis model mice and that GS suppressed the proliferation, migration, and production of proinflammatory cytokines, chemokines and antimicrobial peptides in keratinocytes. Transcriptome analysis by RNA-seq revealed that the differentially expressed genes (DEGs) induced by GS in keratinocytes were intricately linked to the pathogenesis of psoriasis. Furthermore, STAT3, a key player in the development and pathogenesis of psoriasis, was identified as a critical downstream mediator of GS in keratinocytes. Mechanistically, GS upregulated the expression of miR-17-5p, which directly binds to the 3'-untranslated regions (3'UTRs) of JAK1 and STAT3, leading to the downregulation of JAK1 and STAT3 expression. Collectively, these findings suggest that GS may serve as an effective natural compound for the treatment of psoriasis.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116745"},"PeriodicalIF":5.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"JOSD2 promotes breast cancer metastasis by deubiquitinating and stabilizing SMAD4.","authors":"Jiamin Du, Jiao Wang, Fujing Ge, Hongrui Ma, Hongdao Zhu, Jiangxia Du, Fangjie Yan, Qiaojun He, Bo Yang, Tao Yuan, Hong Zhu","doi":"10.1016/j.bcp.2025.116748","DOIUrl":"10.1016/j.bcp.2025.116748","url":null,"abstract":"<p><p>Breast cancer is one of the most common malignant tumors among women worldwide, and its high degree of metastasis significantly impacts treatment effectiveness leading to poor prognosis. The potential molecular mechanisms underlying breast cancer metastasis remain to be further elucidated. In this study, via database analysis, we revealed that the deubiquitinase josephin domain containing 2 (JOSD2) was abnormally amplified in patients with metastatic breast cancer, and was significantly negatively correlated with patient prognosis. By integrating data from the Gene Expression Omnibus (GEO) database and Kyoto Encyclopedia of Genes and Genomes (KEGG) signaling pathway enrichment analysis, we found that the transforming growth factor beta (TGF-β) signaling pathway was significantly activated in breast cancer patients with increased JOSD2 expression. Further studies revealed that JOSD2 interacted with and stabilized SMAD family member 4 (SMAD4) by removing polyubiquitin chains. Inhibition of JOSD2 by RNA interference effectively inhibited the metastasis of breast cancer cells both in vitro and in vivo. In conclusion, our study not only reveals the role of JOSD2 in promoting breast cancer metastasis for the first time, but also indicates promising directions for the future development of deubiquitinase inhibitors, which could yield significant therapeutic benefits. Nevertheless, extensive research and development are required to fully realize this potential.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116748"},"PeriodicalIF":5.3,"publicationDate":"2025-01-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142963686","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cynanchum wallichii Wight and CW1 reversed docetaxel resistance effects by inhibiting P-gp and promoting PI3K/Akt-mediated apoptosis in prostate cancer.","authors":"Qian Feng, Jin-Xiu Zhi, Xue-Yu Wang, Yi-Di Chen, Guan-Cheng Liu, Cai-Yan Wang, Xia Yang, Fang-Ju Feng, Rong Zhang, Zhong-Qiu Liu, Rong-Rong Zhang","doi":"10.1016/j.bcp.2025.116749","DOIUrl":"10.1016/j.bcp.2025.116749","url":null,"abstract":"<p><p>Cynanchum wallichii (CW) is a traditional Chinese medicine which is widely used for treating arthrophlogosis, traumatic injury, and other conditions. Herein, we investigate the effects and mechanisms of CW and its bioactive constituent CW1 in reversing docetaxel (DTX) resistance in prostate cancer (PCa) cells. We investigated the reversal effects of CW and its bioactive constituent CW1 on 22Rv1/DTX cells in vitro and in vivo. We also explored the underlying mechanism by evaluating drug sensitivity, cell proliferation, efflux transporter P-glycoprotein (P-gp), and molecular signaling involved in apoptosis-related protein expression. CW and its bioactive constituent CW1 reversed DTX resistance in PCa 22Rv1/DTX cells by directly binding to the efflux transporter P-gp and by inhibiting the expression of P-gp. This significantly increased the intracellular concentration of DTX and inhibited the malignant proliferation of 22Rv1/DTX cells. In addition, DTX + CW/CW1 co-treatment significantly increased the apoptosis effects in 22Rv1/DTX cells by regulating the relative expressions of BAX, Bcl2, cytochrome C, and caspase 3/9. Furthermore, both CW and CW1 enhanced the in vivo therapeutic effect of DTX in the 22Rv1/DTX cell xenograft while alleviating the side effects of liver and kidney damage caused by DTX. Our results suggest that CW and its bioactive constituent CW1 enhance the antitumor activity of DTX by reducing P-gp expression and promoting phosphoinositide 3-kinase/Akt-mediated apoptosis in vitro and in vivo. Our results firstly confirm that CW1, as a natural bioactive substance, holds promise as an adjuvant drug for treating high-load metastatic and castration-resistant PCa.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116749"},"PeriodicalIF":5.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943650","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"GAS41 promotes ITGA4-mediated PI3K/Akt/mTOR signaling pathway and glioma tumorigenesis.","authors":"Guanglei Shang, Wenju Zhang, Yanjie Jia, Donglei Ji, Enwei Wei, Chunfeng Gao, Caroline Zeng, Chunyu Wang, Nan Liu, Pengfei Ge, Yunqian Li, Lei Zeng","doi":"10.1016/j.bcp.2025.116747","DOIUrl":"10.1016/j.bcp.2025.116747","url":null,"abstract":"<p><p>Glioma Amplified Sequence 41 (GAS41) is a chromatin-associated protein that belongs to the YEATS domain family of proteins and is frequently amplified in various tumors. However, its biological function and carcinogenic mechanism in gliomas are not fully understood. In this study, we revealed that GAS41 was upregulated in human glioma tissues and cell lines, and higher expression of GAS41 was significantly associated with poor clinical prognosis. Genetic depletion and chemical inhibition of GAS41 remarkably inhibited glioma cell proliferation and metastasis abilities and induced cellular apoptosis. Furthermore, functional annotation identified that GAS41 was involved in stimulating the expression of membrane protein ITGA4 to activate the downstream PI3K/Akt/mTOR signaling pathway in glioma cell lines. In addition, we synthesized and evaluated a series of small molecules targeting the GAS41 YEATS domain, which yielded effective anti-proliferative activities in glioma cells. Molecular docking revealed that these compounds bound to the GAS41 YEATS domain pocket in a manner similar to Compounds 9 and 3b, providing a structural basis for exploring the selective inhibition of GAS41 as part of an essential molecular framework. Overall, our study illustrates the crucial role of GAS41 in glioma progression and the malignant phenotype and suggests that targeting GAS41 may be a promising therapeutic treatment strategy for gliomas.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116747"},"PeriodicalIF":5.3,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"CBD and the 5-HT1A receptor: A medicinal and pharmacological review.","authors":"Claire Alexander, Jiyoon Jeon, Kyle Nickerson, Shayne Hassler, Maryam Vasefi","doi":"10.1016/j.bcp.2025.116742","DOIUrl":"10.1016/j.bcp.2025.116742","url":null,"abstract":"<p><p>Cannabidiol (CBD), a phytocannabinoid, has emerged as a promising candidate for addressing a wide array of symptoms. It has the ability to bind to multiple proteins and receptors, including 5-HT1AR, transient receptor potential vanilloid 1 (TRPV1), and cannabinoid receptors. However, CBD's pharmacodynamic interaction with 5-HT1AR and its medicinal outcomes are still debated. This review explores recent literature to elucidate these questions, highlighting the neurotherapeutic outcomes of this pharmacodynamic interaction and proposing a signaling pathway underlying the mechanism by which CBD desensitizes 5-HT1AR signaling. A comprehensive survey of the literature underscores CBD's multifaceted neurotherapeutic effects, which include antidepressant, anxiolytic, neuroprotective, antipsychotic, antiemetic, anti-allodynic, anti-epileptic, anti-degenerative, and addiction-treating properties, attributable in part to its interactions with 5-HT1AR. Furthermore, evidence suggests that the pharmacodynamic interaction between CBD and 5-HT1AR is contingent upon dosage. Moreover, we propose that CBD can induce desensitization of 5-HT1AR via both homologous and heterologous mechanisms. Homologous desensitization involves the recruitment of G protein-coupled receptor kinase 2 (GRK2) and β-arrestin, leading to receptor endocytosis. In contrast, heterologous desensitization is mediated by an elevated intracellular calcium level or activation of protein kinases, such as c-Jun N-terminal kinase (JNK), through the activity of other receptors.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":" ","pages":"116742"},"PeriodicalIF":5.3,"publicationDate":"2025-01-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142943647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of a dual JAK3/TEC family kinase inhibitor for atopic dermatitis therapy.","authors":"Yiwen Du, Longling Wang, Jingmei Zhou, Wenxiang Hong, Xuanyan Cai, Hongbo Ma, Zonghui Wei, Wenwen Nie, Hong Zhu, Bo Yang, Qiaojun He, Binhui Chen, Jiajia Wang, Qinjie Weng","doi":"10.1016/j.bcp.2025.116740","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.116740","url":null,"abstract":"<p><p>Atopic dermatitis (AD) is a chronic inflammatory skin disorder characterized by recurrent eczematous lesions and severe itching, for which clinical treatments are limited. Selectively inhibiting Janus Kinase 3 (JAK3) and tyrosine kinase expressed in hepatocellular carcinoma (TEC) family kinases is proposed as a promising strategy to treat AD with possible reduced side effects and enhanced efficacy. In this study, we developed a dual JAK3/TEC family kinase inhibitor ZZB, which demonstrated potent inhibitory activity with IC₅₀ values of 0.89 nM against JAK3 and 11.56 nM against TEC kinase interleukin-2-inducible T-cell kinase (ITK). Docking studies revealed that ZZB forms a covalent bond with the unique cysteine residue at position 909 (Cys⁹⁰⁹) in JAK3 and Cys⁴⁴² in ITK. Utilizing human peripheral blood mononuclear cells, we discovered ZZB selectively inhibits JAK3-dependent cytokines signaling and ITK-mediated CD4⁺ T cell activation. Moreover, in vitro studies indicated ZZB significantly suppresses the proliferation and differentiation of CD4⁺ T cells, as well as the cytolytic function of CD8⁺ T cells and NK cells. We then conducted a pharmacokinetic study in mice and observed a favorable pharmacokinetic profile for ZZB. In a mouse model of AD induced by repeated application of 2,4-dinitrochlorobenzene to the shaved dorsal skin, oral administration of ZZB (100 mg/kg) markedly improved skin condition and reduced immune cell infiltration, matching the efficacy of the positive drug dexamethasone. We conclude that the JAK3/TEC kinase inhibitor ZZB is a highly promising candidate for the treatment of AD.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"116740"},"PeriodicalIF":5.3,"publicationDate":"2025-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancements in understanding the role and mechanism of sirtuin family (SIRT1-7) in breast cancer management.","authors":"Deepak Sharma, Muthukumaran Panchaksaram, Rajiniraja Muniyan","doi":"10.1016/j.bcp.2025.116743","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.116743","url":null,"abstract":"<p><p>Breast cancer (BC) is the most prevalent type of cancer in women worldwide and it is classified into a few distinct molecular subtypes based on the expression of growth factor and hormone receptors. Though significant progress has been achieved in the search for novel medications through traditional and advanced approaches, still we need more efficacious and reliable treatment options to treat different types and stages of BC. Sirtuins (SIRT1-7) a class III histone deacetylase play a major role in combating various cancers including BC. Studies reveal thateach sirtuin has a unique and well-balanced biology, indicating that it regulates a variety of biological processes that result in the initiation, progression,and metastasis of BC. SIRT also plays a major role in numerous vital biological functions, including apoptosis, axonal protection, transcriptional silencing, DNA recombination and repair, fat mobilization, and aging. As per the current demand, we wish to outline the structural insights into sirtuin's catalytic site, substantial variations among all SIRT types, and their mechanism in BC management. Additionally, this review will focus on the application of SIRT modulators along with their clinical significance, hurdles, and future perspective to develop successful SIRT-based drug candidates to conquer the BC problem.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"116743"},"PeriodicalIF":5.3,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Peptide-based CAR-NK cells: A novel strategy for the treatment of solid tumors.","authors":"Qianqian Wang, Xin Yuan, Cuijuan Liu, Ying Huang, Lin Li, Yimin Zhu","doi":"10.1016/j.bcp.2025.116741","DOIUrl":"https://doi.org/10.1016/j.bcp.2025.116741","url":null,"abstract":"<p><p>CAR-T cell therapy has been proven to be effective on hematological tumors, although graft-versus-host disease and cytokine release syndrome(CRS) limit its application to a certain extent. However, CAR-T therapy for solid tumors met challenges, among which the lack of tumor-specific antigens (TSA) and immunosuppressive tumor microenvironment (TME) are the most important factors. CAR-NK could be a good alternative to CAR-T in some ways since they can induce mild CRS and are independent of HLA-matching, but the efficacy of CAR-NKs remains limited in solid tumors. CAR cells armed with multiple tumor targeting molecules may obtain higher therapeutic efficacy against solid tumors. Due to large molecular weight, multivalent scFvs cannot be displayed efficiently on T cells and the high affinity of scFv to the target makes it easy to cause on-target, off-tumor(OTOT) toxicity. Peptides with low molecular weight and slightly lower affinity than scFvs allow immune cells to display multiple peptides to increase killing ability and reduce OTOT toxicity. In our study, peptide-based CAR-NK cells were designed to solve the dilemma of CAR-T in solid tumors. Firstly, the peptide-based CAR-NK92MI cells with A1 peptide were constructed and their inhibitory effects on the growth of A549 tumor cells were identified. Secondly, the tri-specific CAR-NK92MI cells with peptides that simultaneously targeted PD-L1, EGFR and VEGFR2 were developed for the combinatory therapy. Tri-specific CAR-NK92MI exhibited comparable killing activities to scFv-based CAR-NK92MI. Moreover, peptide-based CAR NK92MI mitigated OTOT toxicity. Our study implied that peptide-based CAR-NKs could behave as promising tools in solid tumor.</p>","PeriodicalId":8806,"journal":{"name":"Biochemical pharmacology","volume":"232 ","pages":"116741"},"PeriodicalIF":5.3,"publicationDate":"2025-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142962163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}