Acta Pharmaceutica Sinica. B最新文献

{"title":"Unlocking the therapeutic potential of RNA splicing in lung fibrosis: Insights from the SRSF7–PKM axis","authors":"Bi-Sen Ding","doi":"10.1016/j.apsb.2025.05.028","DOIUrl":"10.1016/j.apsb.2025.05.028","url":null,"abstract":"","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3351-3352"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472226","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nanomedicine-driven tumor glucose metabolic reprogramming for enhanced cancer immunotherapy","authors":"Chenwei Jiang ,&nbsp;Minglu Tang ,&nbsp;Yun Su ,&nbsp;Junjie Xie ,&nbsp;Qi Shang ,&nbsp;Mingmei Guo ,&nbsp;Xiaoran An ,&nbsp;Longfei Lin ,&nbsp;Ruibin Wang ,&nbsp;Qian Huang ,&nbsp;Guangji Zhang ,&nbsp;Hui Li ,&nbsp;Feihu Wang","doi":"10.1016/j.apsb.2025.04.002","DOIUrl":"10.1016/j.apsb.2025.04.002","url":null,"abstract":"<div><div>Tumors exhibit abnormal glucose metabolism, consuming excessive glucose and excreting lactate, which constructs a tumor microenvironment that facilitates cancer progression and disrupts immunotherapeutic efficacy. Currently, tumor glucose metabolic dysregulation to reshape the immunosuppressive microenvironment and enhance immunotherapy efficacy is emerging as an innovative therapeutic strategy. However, glucose metabolism modulators lack specificity and still face significant challenges in overcoming tumor delivery barriers, microenvironmental complexity, and metabolic heterogeneity, resulting in poor clinical benefit. Nanomedicines, with their ability to selectively target tumors or immune cells, respond to the tumor microenvironment, co-deliver multiple drugs, and facilitate combinatorial therapies, hold significant promise for enhancing immunotherapy through tumor glucose metabolic reprogramming. This review explores the complex interactions between tumor glucose metabolism-specifically metabolite transport, glycolysis processes, and lactate-and the immune microenvironment. We summarize how nanomedicine-mediated reprogramming of tumor glucose metabolism can enhance immunotherapy efficacy and outline the prospects and challenges in this field.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 2845-2866"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471802","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ALKBH3-regulated m1A of ALDOA potentiates glycolysis and doxorubicin resistance of triple negative breast cancer cells","authors":"Yuhua Deng ,&nbsp;Zhiyan Chen ,&nbsp;Peixian Chen ,&nbsp;Yaming Xiong ,&nbsp;Chuling Zhang ,&nbsp;Qiuyuan Wu ,&nbsp;Huiqi Huang ,&nbsp;Shuqing Yang ,&nbsp;Kun Zhang ,&nbsp;Tiancheng He ,&nbsp;Wei Li ,&nbsp;Guolin Ye ,&nbsp;Wei Luo ,&nbsp;Hongsheng Wang ,&nbsp;Dan Zhou","doi":"10.1016/j.apsb.2025.04.018","DOIUrl":"10.1016/j.apsb.2025.04.018","url":null,"abstract":"<div><div>Chemotherapy is currently the mainstay of systemic management for triple-negative breast cancer (TNBC), but chemoresistance significantly impacts patient outcomes. Our research indicates that Doxorubicin (Dox)-resistant TNBC cells exhibit increased glycolysis and ATP generation compared to their parental cells, with this metabolic shift contributing to chemoresistance. We discovered that ALKBH3, an m¹A demethylase enzyme, is crucial in regulating the enhanced glycolysis in Dox-resistant TNBC cells. Knocking down ALKBH3 reduced ATP generation, glucose consumption, and lactate production, implicating its involvement in mediating glycolysis. Further investigation revealed that aldolase A (ALDOA), a key enzyme in glycolysis, is a downstream target of ALKBH3. ALKBH3 regulates <em>ALDOA</em> mRNA stability through m¹A demethylation at the 3′-untranslated region (3′UTR). This methylation negatively affects <em>ALDOA</em> mRNA stability by recruiting the YTHDF2/PAN2–PAN3 complex, leading to mRNA degradation. The ALKBH3/ALDOA axis promotes Dox resistance both <em>in vitro</em> and <em>in vivo</em>. Clinical analysis demonstrated that ALKBH3 and ALDOA are upregulated in breast cancer tissues, and higher expression of these proteins is associated with reduced overall survival in TNBC patients. Our study highlights the role of the ALKBH3/ALDOA axis in contributing to Dox resistance in TNBC cells through regulation of <em>ALDOA</em> mRNA stability and glycolysis.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3092-3106"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SRSF7 promotes pulmonary fibrosis through regulating PKM alternative splicing in lung fibroblasts","authors":"Tongzhu Jin ,&nbsp;Huiying Gao ,&nbsp;Yuquan Wang ,&nbsp;Zhiwei Ning ,&nbsp;Danyang Bing ,&nbsp;Yan Wang ,&nbsp;Yi Chen ,&nbsp;Xiaomu Tian ,&nbsp;Qiudi Liu ,&nbsp;Zhihui Niu ,&nbsp;Jiayu Guo ,&nbsp;Jian Sun ,&nbsp;Ruoxuan Yang ,&nbsp;Qianqian Wang ,&nbsp;Shifen Li ,&nbsp;Tianyu Li ,&nbsp;Yuhong Zhou ,&nbsp;Wenxin He ,&nbsp;Yanjie Lu ,&nbsp;Yunyan Gu ,&nbsp;Haihai Liang","doi":"10.1016/j.apsb.2025.04.017","DOIUrl":"10.1016/j.apsb.2025.04.017","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF), a chronic interstitial lung disease, is characterized by aberrant wound healing, excessive scarring and the formation of myofibroblastic foci. Although the role of alternative splicing (AS) in the pathogenesis of organ fibrosis has garnered increasing attention, its specific contribution to pulmonary fibrosis remains incompletely understood. In this study, we identified an up-regulation of serine/arginine-rich splicing factor 7 (SRSF7) in lung fibroblasts derived from IPF patients and a bleomycin (BLM)-induced mouse model, and further characterized its functional role in both human fetal lung fibroblasts and mice. We demonstrated that enhanced expression of Srsf7 in mice spontaneously induced alveolar collagen accumulation. Mechanistically, we investigated alternative splicing events and revealed that SRSF7 modulates the alternative splicing of pyruvate kinase (PKM), leading to metabolic dysregulation and fibroblast activation. <em>In vivo</em> studies showed that fibroblast-specific knockout of <em>Srsf7</em> in conditional knockout mice conferred resistance to bleomycin-induced pulmonary fibrosis. Importantly, through drug screening, we identified lomitapide as a novel modulator of SRSF7, which effectively mitigated experimental pulmonary fibrosis. Collectively, our findings elucidate a molecular pathway by which SRSF7 drives fibroblast metabolic dysregulation and propose a potential therapeutic strategy for pulmonary fibrosis.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3041-3058"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The crucial function of IDO1 in pulmonary fibrosis: From the perspective of mitochondrial fusion in lung fibroblasts and targeted molecular inhibition","authors":"Lei Wang ,&nbsp;Shanchun Ge ,&nbsp;Ye Zhang ,&nbsp;Deqin Feng ,&nbsp;Ting Zhu ,&nbsp;Louqian Zhang ,&nbsp;Chaofeng Zhang","doi":"10.1016/j.apsb.2025.04.027","DOIUrl":"10.1016/j.apsb.2025.04.027","url":null,"abstract":"<div><div>The pathogenesis of pulmonary fibrosis (PF) is complex. It is characterized by myofibroblast hyperplasia and deposition of collagen protein. Indoleamine 2,3-dioxygenase 1 (IDO1) is expressed in lung fibroblasts and epithelial cells, but its functions in lung homeostasis and diseases remain elusive. Here, we characterize the critical role of IDO1 in PF patients and bleomycin (BLM)-induced PF mouse models. We find that IDO1 is significantly upregulated in the fibrotic lungs of patients and mice, showing a positive correlation with genes characteristic of fibrosis. Functionally, IDO1 knockout inhibits lung fibroblast proliferation, differentiation, mitochondrial biogenesis, and mitochondrial oxidative phosphorylation. Conversely, IDO1 overexpression and accumulation of kynurenine (Kyn) exacerbate progressive lung fibrosis. Mechanistically, IDO1-deletion activated profound mitochondrial fusion-enhanced potentially the capacity for fatty acid oxidation, along with activation of <em>de novo</em> glycolytic serine/glycine synthesis pathways and mitochondrial one-carbon metabolism. Wedelolactone (WEL), a small molecule IKK inhibitor, is found to strongly bind to IDO1 and effectively protect mice from PF in an IDO1-dependent manner. Collectively, this study characterizes a promotor role for IDO1 in PF and suggests a potential avenue of targeting IDO1 to treat lung diseases.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3125-3148"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472293","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Psychological stress-activated NR3C1/NUPR1 axis promotes ovarian tumor metastasis","authors":"Bin Liu ,&nbsp;Wen-Zhe Deng ,&nbsp;Wen-Hua Hu ,&nbsp;Rong-Xi Lu ,&nbsp;Qing-Yu Zhang ,&nbsp;Chen-Feng Gao ,&nbsp;Xiao-Jie Huang ,&nbsp;Wei-Guo Liao ,&nbsp;Jin Gao ,&nbsp;Yang Liu ,&nbsp;Hiroshi Kurihara ,&nbsp;Yi-Fang Li ,&nbsp;Xu-Hui Zhang ,&nbsp;Yan-Ping Wu ,&nbsp;Lei Liang ,&nbsp;Rong-Rong He","doi":"10.1016/j.apsb.2025.04.001","DOIUrl":"10.1016/j.apsb.2025.04.001","url":null,"abstract":"<div><div>Ovarian tumor (OT) is the most lethal form of gynecologic malignancy, with minimal improvements in patient outcomes over the past several decades. Metastasis is the leading cause of ovarian cancer-related deaths, yet the underlying mechanisms remain poorly understood. Psychological stress is known to activate the glucocorticoid receptor (NR3C1), a factor associated with poor prognosis in OT patients. However, the precise mechanisms linking NR3C1 signaling and metastasis have yet to be fully elucidated. In this study, we demonstrate that chronic restraint stress accelerates epithelial–mesenchymal transition (EMT) and metastasis in OT through an NR3C1-dependent mechanism involving nuclear protein 1 (NUPR1). Mechanistically, NR3C1 directly regulates the transcription of NUPR1, which in turn increases the expression of snail family transcriptional repressor 2 (SNAI2), a key driver of EMT. Clinically, elevated NR3C1 positively correlates with NUPR1 expression in OT patients, and both are positively associated with poorer prognosis. Overall, our study identified the NR3C1/NUPR1 axis as a critical regulatory pathway in psychological stress-induced OT metastasis, suggesting a potential therapeutic target for intervention in OT metastasis.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3149-3162"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A chemotherapy nano-booster unlocks wider therapeutic window for prostate cancer treatment","authors":"Rui Liao ,&nbsp;Yuequan Wang ,&nbsp;Ziqi Lin ,&nbsp;Yuting Wang ,&nbsp;Hongyuan Zhang ,&nbsp;Qin Chen ,&nbsp;Shenwu Zhang ,&nbsp;Jin Sun ,&nbsp;Zhonggui He ,&nbsp;Cong Luo","doi":"10.1016/j.apsb.2025.03.029","DOIUrl":"10.1016/j.apsb.2025.03.029","url":null,"abstract":"<div><div>Clinical chemotherapy for prostate cancer is still compromised by high treatment thresholds and severe off-target toxicity of drugs. Given the limited progress in improving therapeutic outcomes and reducing toxicity with the existing toolbox, efforts to broaden the chemotherapeutic window are highly desired. Here, we discover that gossypol (GSP, a natural compound) dramatically enhances the chemosensitivity of cabazitaxel (CTX), even at previously ineffective concentrations. Based on this interesting finding, we exploit a carrier-free chemotherapeutic nano-booster for prostate cancer treatment, which is molecularly co-assembled by GSP and cabazitaxel (CTX). GSP not only readily forms nanoassembly with CTX, but also functions as a chemotherapeutic enhancer that unlocks an ultra-low-dose chemotherapeutic window. Not only that, precise dual-drug nanoassembly confers CTX a significantly larger maximum tolerable dose. As expected, the nano-booster exerts striking therapeutic benefits in mouse prostate tumor xenograft models. This study advances chemotherapeutic window expansion and self-sensitized chemotherapy toward clinical applicability.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3273-3290"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472299","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Silencing PTPN2 with nanoparticle-delivered small interfering RNA remodels tumor microenvironment to sensitize immunotherapy in hepatocellular carcinoma","authors":"Fu Wang ,&nbsp;Haoyu You ,&nbsp;Huahua Liu ,&nbsp;Zhuoran Qi ,&nbsp;Xuan Shi ,&nbsp;Zhiping Jin ,&nbsp;Qingyang Zhong ,&nbsp;Taotao Liu ,&nbsp;Xizhong Shen ,&nbsp;Sergii Rudiuk ,&nbsp;Jimin Zhu ,&nbsp;Tao Sun ,&nbsp;Chen Jiang","doi":"10.1016/j.apsb.2025.03.015","DOIUrl":"10.1016/j.apsb.2025.03.015","url":null,"abstract":"<div><div>Protein tyrosine phosphatase nonreceptor type 2 (PTPN2) is a promising target for sensitizing solid tumors to immune checkpoint blockades. However, the highly polar active sites of PTPN2 hinder drug discovery efforts. Leveraging small interfering RNA (siRNA) technology, we developed a novel glutathione-responsive nano-platform HPssPT (HA/PEIss@si<em>Ptpn2</em>) to silence PTPN2 and enhance immunotherapy efficacy in hepatocellular carcinoma (HCC). HPssPT showed potent transfection and favorable safety profiles. PTPN2 deficiency induced by HPssPT amplified the interferon <em>γ</em> signaling in HCC cells by increasing the phosphorylation of Janus-activated kinase 1 and signal transducer and activator of transcription 1, resulting in enhanced antigen presentation and T cell activation. The nano-platform was also able to promote the M1-like polarization of macrophages <em>in vitro</em>. The unique tropism of HPssPT towards tumor-associated macrophages, facilitated by hyaluronic acid coating and CD44 receptor targeting, allowed for simultaneous reprogramming of both tumor cells and tumor-associated macrophages, thereby synergistically reshaping tumor microenvironment to an immunostimulatory state. In HCC, colorectal cancer, and melanoma animal models, HPssPT monotherapy provoked robust antitumor immunity, thereby sensitizing tumors to PD-1 blockade, which provided new inspiration for siRNA-based drug discovery and tumor immunotherapy.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 2915-2929"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144471855","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design, synthesis and biological evaluation of a novel class of indazole-containing compounds with potent anti-influenza activities targeting the PA-PB1 interface","authors":"Yun-Sang Tang ,&nbsp;Chao Zhang ,&nbsp;Jing Xu ,&nbsp;Haibo Zhang ,&nbsp;Zhe Jin ,&nbsp;Mengjie Xiao ,&nbsp;Nuermila Yiliyaer ,&nbsp;Er-Fang Huang ,&nbsp;Xin Zhao ,&nbsp;Chun Hu ,&nbsp;Pang-Chui Shaw","doi":"10.1016/j.apsb.2025.04.014","DOIUrl":"10.1016/j.apsb.2025.04.014","url":null,"abstract":"<div><div>The PA-PB1 interface of the influenza polymerase is an attractive site for antiviral drug design. In this study, we designed and synthesized a mini-library of indazole-containing compounds based on rational structure-based design to target the PB1-binding interface on PA. Biological evaluation of these compounds through a viral yield reduction assay revealed that compounds <strong>27</strong> and <strong>31</strong> both had a low micromolar range of the half maximal effective concentration (EC₅₀) values against A/WSN/33 (H1N1) (8.03 μmol/L for <strong>27</strong>; 14.6 μmol/L for <strong>31</strong>), while the most potent candidate <strong>24</strong> had an EC₅₀ value of 690 nM. Compound <strong>24</strong> was effective against different influenza strains including a pandemic H1N1 strain and an influenza B strain. Mechanistic studies confirmed that compound <strong>24</strong> bound PA with a <em>K</em>_d which equals to 1.88 μmol/L and disrupted the binding of PB1 to PA. The compound also decreased the lung viral titre in mice. In summary, we have identified a potent anti-influenza candidate with potency comparable to existing drugs and is effective against different viral strains. The therapeutic options for influenza infection have been limited by the occurrence of antiviral resistance, owing to the high mutation rate of viral proteins targeted by available drugs. To alleviate the public health burden of this issue, novel anti-influenza drugs are desired. In this study, we present our discovery of a novel class of indazole-containing compounds which exhibited favourable potency against both influenza A and B viruses. The EC₅₀ of the most potent compounds were within low micromolar to nanomolar concentrations. Furthermore, we show that the mouse lung viral titre decreased due to treatment with compound <strong>24</strong>. Thus our findings identify promising candidates for further development of anti-influenza drugs suitable for clinical use.</div></div>","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3163-3180"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Veronica anagallis-aquatica L. iridoid glycosides alleviate heart failure via metabolites homoveratrumic acid and 2-hydroxy-3,4-dimethoxybenzoic acid mediated by the gut microbiota","authors":"Manjiong Wang ,&nbsp;Xiaobo Guo ,&nbsp;Hanfang Liu ,&nbsp;Xiao Li ,&nbsp;Yue Yao ,&nbsp;Qing Fu ,&nbsp;Yu Jin ,&nbsp;Shuaishuai Ni ,&nbsp;Xiaokang Li ,&nbsp;Chaojiang Xiao ,&nbsp;Bei Jiang ,&nbsp;Conglong Xia ,&nbsp;Jian Li ,&nbsp;Yixiang Xu","doi":"10.1016/j.apsb.2025.04.005","DOIUrl":"10.1016/j.apsb.2025.04.005","url":null,"abstract":"","PeriodicalId":6906,"journal":{"name":"Acta Pharmaceutica Sinica. B","volume":"15 6","pages":"Pages 3338-3342"},"PeriodicalIF":14.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144472222","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}