European journal of pharmacology最新文献

{"title":"Neuroprotective Effect of Perillyl alcohol in Sporadic Alzheimer's disease in Rats.","authors":"Dolly Chauhan, Kajal Bagri, Rahul Deshmukh","doi":"10.1016/j.ejphar.2025.177558","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177558","url":null,"abstract":"<p><p>As people age, Alzheimer's disease, a neurological disorder that develops gradually, affects their memory and cognitive abilities. The two hallmarks of Alzheimer's disease are intracellular buildup of neurofibrillary tangles and extracellular β-amyloid plaques. In this work, the effects of Perillyl alcohol on experimental sporadic Alzheimer-type dementia produced by intracerebroventricular streptozotocin were investigated. Rats that received streptozotocin infusion experienced cholinergic hypofunction, increased oxidative-nitritive stress, and impaired memory and learning. Between 15 and 27 days following the initial streptozotocin infusion, 13 days of treatment with Perillyl alcohol (25, 50, and 100 mg/kg p.o.) significantly improved learning and memory in Morris water maze and object recognition test paradigms. Perillyl also significantly reduced oxidative-nitritive stress, as seen by a decrease in malondialdehyde and nitrite, and restored reduced glutathione and catalase levels. Acetylcholinesterase activity significantly increased in the current model, indicating cholinergic hypofunction and enhanced neuronal cell damage. Treatment with Perillyl alcohol also significantly decreased the increase in acetylcholinesterase activity, indicating that Perillyl alcohol may be able to prevent neuronal damage and restore cholinergic functions. Perillyl alcohol has been shown to improve spatial memory processing, which may be due to its antioxidant properties and capacity to restore cholinergic functioning. However, more study is required to understand the molecular mechanisms of POH that enhance cognition or prevent neurotoxic damage, which could support its application in neuroprotective effect.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177558"},"PeriodicalIF":4.2,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling EIF5A2: A Multifaceted Player in Cellular Regulation, Tumorigenesis and Drug Resistance.","authors":"Xifeng Xiong, Yanli Du, Peng Liu, Xinye Li, Xudong Lai, Haixiong Miao, Bo Ning","doi":"10.1016/j.ejphar.2025.177596","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177596","url":null,"abstract":"<p><p>The eukaryotic initiation factor 5A2 gene (EIF5A2) is a highly conserved and multifunctional gene that significantly influences various cellular processes, including translation elongation, RNA binding, ribosome binding, protein binding and post-translational modifications. Overexpression of EIF5A2 is frequently observed in multiple cancers, where it functions as an oncoprotein. Additionally, EIF5A2 is implicated in drug resistance through the regulation of various molecular pathways. In the review, we describe the structure and functions of EIF5A2 in normal cells and its role in tumorigenesis. We also elucidate the molecular mechanisms associated with EIF5A2 in the context of tumorigenesis and drug resistance. We propose that the biological roles of EIF5A2 in regulating diverse cellular processes and tumorigenesis are clinically significant and warrant further investigation.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177596"},"PeriodicalIF":4.2,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802887","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Eco-Friendly Nanotherapeutics: Metallic Nanoparticles for Targeting Breast Cancer.","authors":"Darakhshan Javaid, Shahid Yousuf Ganie, Syed Sanober Qadri, Adfar Reyaz, Mohd Salim Reshi","doi":"10.1016/j.ejphar.2025.177603","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177603","url":null,"abstract":"<p><p>Breast cancer continues to be a major cause of death among women globally, with triple-negative breast cancer (TNBC) presenting a particularly difficult challenge due to its aggressive behaviour and the lack of effective treatment options. Nanotechnology, particularly the use of silver nanoparticles (AgNPs), has emerged as a promising avenue in oncological research. This review explores into the escalating field of green synthesis of nanoparticles, emphasizing sustainable approaches utilizing plant-based resources. Critical factors influencing nanoparticle synthesis, including reaction conditions, precursor types, and plant phytochemicals, are explored alongside advanced characterization techniques essential for evaluating nanoparticle properties. Special focus is given to the phytofabrication of silver nanoparticles and their multifaceted roles in breast cancer treatment, with detailed insights into their mechanisms, such as inducing apoptosis, generating reactive oxygen species (ROS), and disrupting mitochondrial function, particularly in TNBC cells. The review further highlights the advantages of plant-derived AgNPs, such as biocompatibility and reduced toxicity, while addressing challenges like scalability, reproducibility, and regulatory hurdles. Concluding with future prospects, this paper reflects the potential of green-synthesized AgNPs as a keystone in next-generation cancer therapeutics, paving the way for innovative and eco-friendly approaches in oncology.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177603"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biostability, in vivo antiviral activity against respiratory syncytial virus, and pharmacokinetic profiles of (−)-borneol esters","authors":"Anastasiya S. Sokolova ,&nbsp;Alina A. Okhina ,&nbsp;Anna A. Shtro ,&nbsp;Artem M. Klabukov ,&nbsp;Anastasia V. Galochkina ,&nbsp;Yulia V. Nikolaeva ,&nbsp;Galina D. Petukhova ,&nbsp;Olga I. Yarovaya ,&nbsp;Artem D. Rogachev ,&nbsp;Dmitriy S. Baev ,&nbsp;Alina V. Fatyanova ,&nbsp;Tatyana G. Tolstikova ,&nbsp;Nariman F. Salakhutdinov","doi":"10.1016/j.ejphar.2025.177567","DOIUrl":"10.1016/j.ejphar.2025.177567","url":null,"abstract":"<div><div>Respiratory syncytial virus (RSV) is a leading cause of severe lower respiratory tract infections, particularly in vulnerable populations such as infants and the elderly. In this study, we evaluated the metabolic stability, <em>in vivo</em> antiviral activity, and pharmacokinetic profiles of (−)-borneol esters, which were identified as potent RSV inhibitors through screening of a compound library. Two hit compounds, ST-2 and AS-645, caused a reduction in viral titers in RSV-infected mice. Intranasal administration of ST-2 proved more effective than oral one and showed enhanced antiviral activity and improved pharmacokinetic properties. Additionally, ST-2 manifested superior metabolic stability in human blood compared to murine and rat blood, suggesting that carboxylesterase activity is a key factor in the hydrolysis resistance. Given that carboxylesterase activity is higher in mouse blood than in human blood, this difference likely contributes to the observed stability of ST-2 in human blood. Molecular modeling confirmed the role of carboxylesterase in the hydrolysis of (−)-borneol esters. These findings suggest that ST-2 has potential for further development of drugs for RSV and other viral infections.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"996 ","pages":"Article 177567"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The sodium-glucose cotransporter 2 inhibitor tofogliflozin induces vasodilation of rabbit femoral artery by activating Kv channels, the SERCA pump, and the sGC/cGMP pathway","authors":"Wenwen Zhuang ,&nbsp;Minju Park ,&nbsp;Junsu Jeong ,&nbsp;Hye Ryung Kim ,&nbsp;YeEun Jang ,&nbsp;Mi Seon Seo ,&nbsp;Jin Ryeol An ,&nbsp;Hongzoo Park ,&nbsp;Won-Kyo Jung ,&nbsp;Il-Whan Choi ,&nbsp;Won Sun Park","doi":"10.1016/j.ejphar.2025.177595","DOIUrl":"10.1016/j.ejphar.2025.177595","url":null,"abstract":"<div><div>Tofogliflozin is a sodium-glucose cotransporter 2 inhibitor widely used to treat type 2 diabetes mellitus, but it also exhibits cardio-protective effects. This study investigated the vasodilatory action of tofogliflozin using rabbit femoral artery rings pre-contracted with phenylephrine (1 μM). The results showed the concentration-dependent induction of vasodilation by tofogliflozin, a response that remained unchanged following endothelial removal, pretreatment with the nitric oxide synthase inhibitor L-NAME (100 μM), or the inhibition of low- and intermediate-conductance Ca²⁺-activated K⁺ channels using apamin (1 μM) in combination with TRAM-34 (1 μM). Furthermore, pretreatment with the voltage-dependent K⁺ (Kv) channel inhibitor 4-AP (3 mM) reduced the vasodilatory effects of tofogliflozin whereas pretreatment with the ATP-sensitive K⁺ channel inhibitor glibenclamide (10 μM) or the large-conductance Ca²⁺-activated K⁺ channel inhibitor paxilline (1 μM) did not. Notably, our findings indicated that Kv7.X, rather than Kv1.5 or Kv2.1, is the primary Kv subtype involved in tofogliflozin-induced vasodilation. The vasodilatory effects of tofogliflozin were also significantly inhibited in femoral arterial rings pretreated with the sarco/endoplasmic reticulum Ca²⁺-ATPase (SERCA) pump inhibitors thapsigargin (1 μM) and cyclopiazonic acid (10 μM). Tofogliflozin-induced vasodilation was unaltered in arterial rings exposed to the adenylyl cyclase inhibitor SQ 22536 (50 μM), the protein kinase A (PKA) inhibitor KT 5720 (1 μM), and the protein kinase G inhibitor KT 5823 (1 μM) whereas it was effectively reduced by the soluble guanylyl cyclase (sGC) inhibitor ODQ (10 μM). These findings suggest that tofogliflozin-induced vasodilation is mediated by the activation of the SERCA pump, the sGC/cGMP pathway, and Kv channels.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"996 ","pages":"Article 177595"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143792309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dipeptidyl Peptidase 3 Induces Myocardial Ischemia-Reperfusion Injury by Mediating Mitophagy and the Intrinsic Apoptotic Pathway.","authors":"Xiao Wang, Yaofeng Xie, Hongjiao Du, Cheng Chang, Chunyang Tian, Yuyao Yin, Xiaodong Li, Yilong Pan","doi":"10.1016/j.ejphar.2025.177592","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177592","url":null,"abstract":"<p><strong>Background: </strong>Dipeptidyl peptidase 3 (DPP3) is a zinc-dependent hydrolase that is regarded as a \"myocardial inhibitor\". However, the role of DPP3 in myocardial ischemia-reperfusion injury (MIRI) remain to be investigated. The present study aimed to investigate the potential role of DPP3 in MIRI and elucidate the underlying mechanisms.</p><p><strong>Methods: </strong>The AC16 cardiomyocyte cell line was used to investigate the interactions between DPP3 and its protein interactors, and assess its effects on the apoptosis of cardiomyocytes following oxygen glucose deprivation/reperfusion (OGD/R) treatment in vitro. An animal model of ischemia/reperfusion (I/R) injury was established using C57BL/6J mice for in vivo analyses. The role of DPP3 and the underlying mechanisms were investigated both in vitro and in vivo following DPP3 knockdown and overexpression.</p><p><strong>Results: </strong>DPP3 interacted with Parkinson's disease protein 7 (Park7), and DPP3 overexpression altered the expression levels of proteins related to the intrinsic apoptotic pathway and autophagy. This significantly downregulated the mitochondrial expression of cytochrome C, thereby exacerbating mitochondrial injury and increasing the rate of apoptosis following reperfusion. DPP3 knockdown reversed these effects; however, the simultaneous knockdown of DPP3 and Park7 did not confer the beneficial effects observed with DPP3 knockdown alone. DPP3 knockdown alleviated the extent of myocardial injury and improved cardiac function in the mouse model of I/R injury.</p><p><strong>Conclusions: </strong>The study demonstrated that DPP3 mediates mitophagy and apoptosis in MIRI through its interaction with Park7. These findings have important implications, suggesting that targeting DPP3 and its associated signaling pathways may serve as a potential therapeutic strategy, and that the downregulation of DPP3 can potentially alleviate MIRI.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177592"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794554","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fisetin and resveratrol exhibit senotherapeuticeffects and suppress cellular senescence in osteoarthritic cartilage-derived chondrogenic progenitor cells.","authors":"Justin Jacob, Aditya Aggarwal, Shalmoli Bhattacharyya, Daisy Sahni, Vinit Sharma, Anjali Aggarwal","doi":"10.1016/j.ejphar.2025.177573","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177573","url":null,"abstract":"<p><p>Chondrogenic progenitor cells (CPCs) in the articular cartilage of knee osteoarthritis (OA) patients exhibit cellular senescence and its associated secretory phenotype (SASP).We hypothesized that the senescence of CPCs can be suppressed using natural compounds. This study aimed to evaluate the senotherapeutic effects offisetin and resveratrol to suppress the cellular senescence inCPCs. In vitro, pre-treatment of CPCs with increasing doses of fisetin and resveratrol (5μM-100μM) were non-cytotoxic, decreased senescence index and dampened the expression of cellular senescencemarkers,p53 and p38MAPK. Additionally, SASP-related genes and proteins (MMP-9, MMP13) and inflammatory mediators (IL-1β, TGF-β, and IL-6) were downregulated. Further,in silico analysis confirmed the high binding affinity of these natural drugs to OA-related proteins. Overall, fisetin and resveratrol dampened the senescence of CPCs by downregulating the p53 effector protein and effectively reduced theSASP. From this study,natural compound candidates proved to be potential drug candidates that suppress senescence via p53.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177573"},"PeriodicalIF":4.2,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143794773","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"FKBP5 mediates glucocorticoid signaling in estrogen deficiency-associated endothelial dysfunction","authors":"Ruiwen Zhu ,&nbsp;Yiyue Xu ,&nbsp;Huixian Li ,&nbsp;Chufeng He ,&nbsp;Fung Ping Leung ,&nbsp;Lin Wang ,&nbsp;Wing Tak Wong","doi":"10.1016/j.ejphar.2025.177598","DOIUrl":"10.1016/j.ejphar.2025.177598","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular disease (CVD) is the leading cause of mortality among postmenopausal women, with atherosclerosis being a major underlying factor. Endothelial dysfunction, a key initiating event in atherosclerosis, can be triggered by hormonal and metabolic changes. While estrogen deficiency has been linked to increased cardiovascular risk, the molecular mechanisms by which it exacerbates endothelial dysfunction, particularly in the presence of elevated glucocorticoid levels, remain poorly understood. This study aims to explore the role of FK506-binding protein 5 (FKBP5) in mediating glucocorticoid-induced endothelial dysfunction in estrogen-deficient females.</div></div><div><h3>Methods</h3><div>Estrogen deficiency was developed in female mice by ovariectomy (OVX). Female mice and human umbilical vein endothelial cells (HUVECs) were treated with dexamethasone (DEX) to mimic elevated cortisol levels <em>in vivo</em> and <em>vitro</em>. Endothelial function of the mice aorta was assessed using wire myography. Oxidative stress and inflammation were evaluated through reactive oxygen species (ROS) detection, immunofluorescence and mRNA expression analysis. The selective FKBP5 inhibitor SAFit2 was used to study the functional role of FKBP5 in these processes.</div></div><div><h3>Results</h3><div>Estrogen deficiency contributed to endothelial dysfunction in female mice, an effect exacerbated by elevated glucocorticoid levels. FKBP5 expression was upregulated in both ovariectomized mice aortas and DEX-treated endothelial cells. Inhibition of FKBP5 reversed endothelial dysfunction, reduced ROS levels, and suppressed the expression of pro-inflammatory mediators, including ICAM-1, IL-1β, TNF-α, and NF-κB.</div></div><div><h3>Conclusion</h3><div>FKBP5 mediates glucocorticoid-induced endothelial dysfunction under estrogen-deficient conditions. Inhibition of FKBP5 represents a promising therapeutic strategy to ameliorate endothelial dysfunction and improve vascular health in estrogen-deficient women.</div></div>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":"996 ","pages":"Article 177598"},"PeriodicalIF":4.2,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143785964","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of decrease in Klotho protein expression on insulin signaling and levels of proteins related to brain energy metabolism.","authors":"Ana Maria Marques Orellana, Caio Henrique Mazucanti, Diana Zukas Andreotti, Larissa de Sá Lima, Elisa Mitiko Kawamoto, Cristoforo Scavone","doi":"10.1016/j.ejphar.2025.177587","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177587","url":null,"abstract":"<p><p>Mutations in Klotho have been associated with premature ageing and cognitive dysfunction. Although highly expressed in specific regions of the brain, the actions of Klotho in the central nervous system (CNS) remain largely unknown. Here, we show that animals with a mutated hypomorphic Klotho gene have altered glycaemic regulation, suggesting higher insulin sensitivity. In the CNS, pathways related to insulin intracellular signalling were found to be up-regulated in the hippocampus, with higher activation of protein kinase B and mammalian target of rapamycin and inactivation of the transcription factors forkhead box O (FOXO)-1 and FOXO-3a. In addition, the present study showed that in the hippocampi of wild-type aged mice, where Klotho is naturally downregulated, the levels of some proteins related to energy metabolism and metabolic coupling between neurones and astrocytes, such as monocarboxylate transporter 2 and 4, 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase isoform 3 and lactate dehydrogenase enzymes isoforms A and B were altered. These findings suggest that Klotho plays an essential role in regulating proteins and genes related to metabolic coupling in the brain.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177587"},"PeriodicalIF":4.2,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788241","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The protective effect of amylin in type 2 diabetes: Yes or no.","authors":"Mansour Alanazi, Hayder M Al-Kuraishy, Ali K Albuhadily, Ali I Al-Gareeb, Ahmed M Abdelaziz, Athanasios Alexiou, Marios Papadakis, Gaber El-Saber Batiha","doi":"10.1016/j.ejphar.2025.177593","DOIUrl":"https://doi.org/10.1016/j.ejphar.2025.177593","url":null,"abstract":"<p><p>Amylin, which is also called a human islet amyloid polypeptide, is a peptide hormone made up of 37 amino acids that is released from pancreatic β cells. It helps keep blood sugar levels stable by controlling the release of insulin and glucagon. Various studies have indicated its involvement in the pathogenesis of type 2 diabetes (T2D) through the induction of apoptosis in pancreatic cells. Conversely, other studies found that amylin plays a critical role in the pathogenesis of T2D by affecting the release of insulin and glucagon. Therefore, amylin has protective and detrimental effects on the pathogenesis of T2D. Consequently, this review aims to discuss the beneficial and detrimental roles of amylin in T2D.</p>","PeriodicalId":12004,"journal":{"name":"European journal of pharmacology","volume":" ","pages":"177593"},"PeriodicalIF":4.2,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}