Biomolecules & Therapeutics最新文献_第2页

Arrestins as Possible Drug Targets. 逮捕是可能的毒品目标。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-06 DOI: 10.4062/biomolther.2025.079

Zeynep Nur Cinviz, Elisabetta Moroni, Ozge Sensoy, Giulia Morra, Vsevolod V Gurevich

引用次数: 0

Pathophysiological Insights and Clinical Management Strategies for Interstitial Lung Diseases. 间质性肺疾病的病理生理学见解和临床管理策略。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-14 DOI: 10.4062/biomolther.2025.003

Lin Tian, Yun Wang, Wenlong Qi, Bingsen Wang, Xudong Zhang, Mingxue Gong, Xiang Zhang, Tan Wang

{"title":"Pathophysiological Insights and Clinical Management Strategies for Interstitial Lung Diseases.","authors":"Lin Tian, Yun Wang, Wenlong Qi, Bingsen Wang, Xudong Zhang, Mingxue Gong, Xiang Zhang, Tan Wang","doi":"10.4062/biomolther.2025.003","DOIUrl":"10.4062/biomolther.2025.003","url":null,"abstract":"Interstitial lung disease (ILD) represents a heterogeneous group of diseases in which inflammation and/or fibrosis in the pulmonary interstitium results in an impaired gas exchange, difficulties in breathing, and reduced quality of daily life, and contributes to elevated global morbidity and mortality rates. ILD is an umbrella term, with idiopathic pulmonary fibrosis (IPF) being a prime focus because of its progressive and severe form. Out of 300 underlying etiologies, ILD is one of the major reasons for global morbidity and mortality. This review offers a comprehensive overview of six main categories of ILD covering autoimmune, idiopathic interstitial pneumonia, hypersensitivity pneumonitis, drug-induced, infection-related, and unclassified ILD that underscore the complexity of diagnosis and treatment challenges. This review also provides an evidence-based overview of recent advancements in the diagnosis and management of ILD, with precision pharmacotherapy, multidisciplinary care, and emerging therapeutic strategies. From clinical trial data, it also recommends the disease-specific use of pharmacological agents-such as pirfenidone and nintedanib for IPF, and mycophenolate mofetil for connective tissue disease-associated ILD. The manuscript also emphasizes the evolving role of non-pharmacological interventions, including the 6-minute walk test and pulmonary rehabilitation, in enhancing functional capacity and quality of life. To address the current global health concerns, topics of post-COVID-19 ILD and immune checkpoint inhibitor-associated lung disease are integrated. Additionally, future directions are explored, including the role of lung transplantation and novel antifibrotic therapies like anti-Transforming Growth Factor (TGF)-β antibody cocktails. Together, these insights aim to refine diagnostic precision, personalize treatment, and improve clinical outcomes across the heterogeneous ILD spectrum.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"785-803"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408203/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144844326","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}

引用次数: 0

Xylene Impairs Neuronal Development by Dysregulating Calcium Homeostasis and Neuronal Activity in Developing Hippocampal Neurons. 二甲苯通过调节发育中的海马神经元钙稳态和神经元活动而损害神经元发育。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-31 DOI: 10.4062/biomolther.2025.038

Yunkyung Eom, Sung Hoon Lee

{"title":"Xylene Impairs Neuronal Development by Dysregulating Calcium Homeostasis and Neuronal Activity in Developing Hippocampal Neurons.","authors":"Yunkyung Eom, Sung Hoon Lee","doi":"10.4062/biomolther.2025.038","DOIUrl":"10.4062/biomolther.2025.038","url":null,"abstract":"Xylene is an aromatic hydrocarbon widely used as a solvent and emitted from numerous commercial products in industrial or indoor settings. Epidemiological studies of occupational exposure indicate that xylene primarily targets the central nervous system, producing neurobehavioral impairments and other neurological disorders. Both environmental and occupational exposure to volatile organic compounds, therefore, raise concerns about neurodevelopmental risk; however, the specific neurotoxicity of xylene in developing neurons remains poorly characterized. Here, we investigated the effects of xylene (2 or 5 mM) on developing mouse hippocampal neurons, with a focus on Ca2+ homeostasis, presynaptic function, and electrophysiological activity. We assessed Ca2+ homeostasis with selective inhibitors of voltage-gated Ca2+ channels and organelle-specific Ca2+ indicators. Presynaptic activity was evaluated in transgenic mouse pups expressing a genetically encoded pH sensor within the synaptic vesicle lumen. Xylene suppressed cytosolic Ca2+ transients by inhibiting P/Q-type Ca2+ channels, thereby reducing Ca2+ uptake into the endoplasmic reticulum. It also decreased Ca2+ influx at both presynaptic and postsynaptic sites, impairing synaptic vesicle exocytosis and endocytosis. Electrophysiological and morphological analyses further showed reduced spontaneous firing and hindered synaptic maturation. Collectively, these findings provide mechanistic insight into the neurotoxic actions of xylene and underscore its potential hazard to brain development and function.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"33 5","pages":"830-841"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408200/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941392","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}

引用次数: 0

trans-Resveratrol and Hesperidin Supplementation with Treadmill Exercise Alleviates Methylglyoxal-Induced Skeletal Muscle Dysfunction. 在跑步机运动中补充反式白藜芦醇和橙皮苷可减轻甲基乙二醛诱导的骨骼肌功能障碍。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-31 DOI: 10.4062/biomolther.2025.018

Jinho Park, Seong-Min Hong, Jiyoun Kim, Sun Yeou Kim

{"title":"trans-Resveratrol and Hesperidin Supplementation with Treadmill Exercise Alleviates Methylglyoxal-Induced Skeletal Muscle Dysfunction.","authors":"Jinho Park, Seong-Min Hong, Jiyoun Kim, Sun Yeou Kim","doi":"10.4062/biomolther.2025.018","DOIUrl":"10.4062/biomolther.2025.018","url":null,"abstract":"Methylglyoxal (MGO), a reactive glycolytic byproduct, contributes to skeletal muscle atrophy by promoting oxidative stress, inflammation, and protein degradation. This study investigated the therapeutic potential of trans-resveratrol and hesperidin (tRES-HESP) supplementation, alone or in combination with aerobic exercise, in ameliorating MGO-induced muscle dysfunction in mice. ICR mice were divided into five groups and treated with MGO, tRES-HESP, treadmill exercise, or both interventions over eight weeks. Muscle mass, grip strength, endurance performance, histopathology, and molecular biomarkers were assessed. Combined treatment with tRES-HESP and exercise significantly improved muscle function and morphology, restored muscle mass, and suppressed fibrosis. In terms of signaling pathways, the protective effects were associated with activation of the AMPK/SIRT1/PGC-1α pathway for mitochondrial biogenesis, stimulation of the AKT/mTOR pathway for muscle protein synthesis, suppression of MuRF1-mediated protein degradation, and upregulation of MyoD and MyHC, key markers of muscle regeneration and structural integrity. Additionally, inflammatory balance was restored via suppression of pro-inflammatory IL-6 and elevation of anti-inflammatory IL-10 levels. These findings highlight the synergistic benefits of combining polyphenol supplementation with aerobic exercise as a promising strategy for mitigating muscle atrophy under metabolic stress conditions.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"33 5","pages":"890-900"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408198/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144941458","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}

引用次数: 0

Atopic Dermatitis Management: from Conventional Therapies to Biomarker-Driven Treatment Approaches. 特应性皮炎管理：从传统疗法到生物标志物驱动的治疗方法。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-19 DOI: 10.4062/biomolther.2025.081

Hye Won Lee, Yun Jin Ju, Seeun Choi, Kiyon Rhew, Samantha Serafin Sevilleno, Min Sik Choi

{"title":"Atopic Dermatitis Management: from Conventional Therapies to Biomarker-Driven Treatment Approaches.","authors":"Hye Won Lee, Yun Jin Ju, Seeun Choi, Kiyon Rhew, Samantha Serafin Sevilleno, Min Sik Choi","doi":"10.4062/biomolther.2025.081","DOIUrl":"10.4062/biomolther.2025.081","url":null,"abstract":"Atopic dermatitis (AD) is a chronic relapsing inflammatory skin disorder characterized by pruritus, skin barrier dysfunction, and immune dysregulation. It significantly impacts the quality of life and increases the risk of infections, sleep disturbances, and psychological distress. AD pathogenesis involves genetic predisposition, environmental triggers, microbiome alterations, and immune dysfunction. Traditional treatments such as topical corticosteroids, calcineurin inhibitors, and systemic immunosuppressants provide symptomatic relief but often fail to provide long-term disease control. The emergence of targeted biologics and Janus kinase inhibitors has transformed AD management by offering more precise and effective therapeutic options. However, treatment responses vary, highlighting the need for biomarker-driven personalized therapies. In this review, we explore the evolving therapeutic landscape of AD, emphasizing the emerging role of biomarker-guided treatment strategies. We highlight recent discoveries of therapeutic (OX40, IgE, IL-5, IL-31, IL-22, thymic stromal lymphopoietin) and diagnostic (TARC/CCL17, MDC/CCL2, filaggrin, sphingosine-1-phosphate, CXCL2) biomarkers that offer promising avenues for patient stratification and treatment monitoring. This review offers novel insight into how the convergence of biomarker research and therapeutic innovation can address current gaps in AD care. Future research should focus on refining biomarker-guided treatment strategies, optimizing therapeutic combinations, and addressing unmet patient needs. The integration of biomarker-guided strategies into routine clinical practice represents a critical step toward long-term disease control and improved quality of life for AD patients.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"813-829"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408207/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871264","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}

引用次数: 0

An Endolichenic Fungi-Derived Fatty Acid, cis-10-Nonadecenoic acid, Suppresses Colorectal Cancer Stemness. 一种内生真菌衍生的脂肪酸，顺式-10-壬烯酸，抑制结直肠癌的发生。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-06 DOI: 10.4062/biomolther.2025.062

Mücahit Varlı, Eun-Young Lee, So-Yeon Park, Yi Yang, Prima F Hillman, Rui Zhou, Jae-Seoun Hur, Sang-Jip Nam, Hangun Kim

{"title":"An Endolichenic Fungi-Derived Fatty Acid, cis-10-Nonadecenoic acid, Suppresses Colorectal Cancer Stemness.","authors":"Mücahit Varlı, Eun-Young Lee, So-Yeon Park, Yi Yang, Prima F Hillman, Rui Zhou, Jae-Seoun Hur, Sang-Jip Nam, Hangun Kim","doi":"10.4062/biomolther.2025.062","DOIUrl":"10.4062/biomolther.2025.062","url":null,"abstract":"Endolichenic fungi (ELF), symbionts of lichens, have been reported to produce diverse bioactive secondary metabolites with promising pharmaceutical potential. In this study, we isolated and identified an ELF, EL001668 (KACC 83020BP), from Cetraria laevigata Rass., and assessed its crude extract and bioactive compounds against colorectal cancer (CRC) stem cell activity. cis-10-nonadecenoic acid (c-NDA), isolated through bioactivity-guided fractionation exerted substantial inhibitory effects on CRC stemness, such as the suppression of spheroid formation and the downregulation of the key stem cell markers ALDH1, CD44, and CD133. Comparative analysis with the omega-3 fatty acids EPA and DHA, with well-established properties, showed that c- NDA exerted comparable or superior inhibitory effects against the markers and phenotypic traits of stemness. Besides, the crude extract of EL001668 exhibited greater suppression of certain markers in comparison to the individual compounds. These findings suggest that c-NDA, in conjunction with ELF-derived compounds, holds potential as a novel therapeutic candidate targeting CRC stem cells. Taken together, the current study demonstrated that c-NDA, similar to EPA and DHA, may possess adjunct or complementary effects in cancer treatment and other diseases.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"842-851"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408206/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144788178","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}

引用次数: 0

Understanding Tumor Dormancy: from Experimental Models to Mechanisms and Therapeutic Strategies. 了解肿瘤休眠：从实验模型到机制和治疗策略。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-31 DOI: 10.4062/biomolther.2025.056

Jaebeom Cho

引用次数: 0

Control of Overly Secreted Tryptophanyl tRNA Synthetase Attenuates Sepsis Severity in a Porcine Model. 控制过度分泌色氨酸tRNA合成酶可减轻猪模型脓毒症的严重程度。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-13 DOI: 10.4062/biomolther.2025.071

Yoon Tae Kim, Geunyeol Jeong, Yihyo Kim, HyeonJu Roh, Susung Lim, Jinah Jang, Yun Hui Choi, Kyoung Chul Park, Mirim Jin

{"title":"Control of Overly Secreted Tryptophanyl tRNA Synthetase Attenuates Sepsis Severity in a Porcine Model.","authors":"Yoon Tae Kim, Geunyeol Jeong, Yihyo Kim, HyeonJu Roh, Susung Lim, Jinah Jang, Yun Hui Choi, Kyoung Chul Park, Mirim Jin","doi":"10.4062/biomolther.2025.071","DOIUrl":"10.4062/biomolther.2025.071","url":null,"abstract":"Sepsis is a leading cause of mortality in hospitals with a lack of reliable biomarkers and specialized therapeutics. Recently, highly secreted tryptophanyl-tRNA synthetase 1 (WARS1), an endogenous ligand for Toll-like receptor (TLR) 2 and TLR4, was found to be a potential theranostic target for hypercytokinemic severe sepsis. In this study, using the minipig sepsis model inoculated with cecum slurry, we demonstrated that increases in WARS1 levels were associated with severity of sepsis and showed strong correlations with RBC count and the levels of HGB, HCT, EPO, lactate, and PLT count in the acute phase of sepsis. Further, administration of the WARS1 neutralizing antibody to the septic minipigs inhibited the increase in the overall SOFA score with a significantly lower P/F ratio, which was accompanied by the suppression of proinflammatory cytokine and chemokine expressions as well as EPO production, a decrease in AST and ALT levels, and inflammatory immune cell infiltration in the lung. Taken together, these findings provide a novel insight into the pathophysiology of acute phase of sepsis and suggest the clinical application of WARS1 neutralizing therapeutics in the treatment of sepsis.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"852-865"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833846","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}

引用次数: 0

Melatonin Prevents the Progression of MASLD via Inhibiting FFAs-Induced Ferroptosis through KEAP1/NRF2/HO-1 Pathway. 褪黑素通过KEAP1/NRF2/HO-1通路抑制ffas诱导的铁下垂，从而阻止MASLD的进展。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-18 DOI: 10.4062/biomolther.2025.037

Shuojiao Li, Peng Rao, Wenxian Yu, Yue Tang, Xuanpeng Jiang, Jiatao Liu

{"title":"Melatonin Prevents the Progression of MASLD via Inhibiting FFAs-Induced Ferroptosis through KEAP1/NRF2/HO-1 Pathway.","authors":"Shuojiao Li, Peng Rao, Wenxian Yu, Yue Tang, Xuanpeng Jiang, Jiatao Liu","doi":"10.4062/biomolther.2025.037","DOIUrl":"10.4062/biomolther.2025.037","url":null,"abstract":"The accumulation of free fatty acids (FFAs) in hepatocytes is a key characteristic of metabolic dysfunction-associated steatotic liver disease (MASLD), which leads to lipid peroxidation and ultimately results in ferroptosis. Currently, there is an absence of efficacious therapeutic options available for the management of MASLD. Consequently, an in-depth exploration of the roles of FFAs and ferroptosis in the progression of MASLD may reveal hitherto unidentified therapeutic targets. In the study, we established an early lesion model of MASLD, namely NAFL, and comprehensive analyses of lipid metabolism, hepatocellular injury, iron homeostasis, and ferroptosis were performed. The HFD and FFAs treatment significantly elevated the expression of enzymes associated with lipid synthesis, including ACC1 and FASN, leading to enhanced lipid accumulation in hepatocytes. Additionally, HFD and FFAs resulted in increased iron loading and a reduction in the levels of the antioxidant enzyme GPX4, which ultimately triggers ferroptosis. In contrast, the administration of melatonin effectively inhibited the activity of lipid synthesis-related enzymes, decreased hepatic lipid deposition, alleviated free fatty acid-induced iron dysregulation, and mitigated liver damage. Mechanistically, melatonin has been shown to attenuate hepatocyte ferroptosis by modulating the KEAP1/NRF2/HO-1 pathway, which in turn diminishes free fatty acids-induced oxidative stress. In conclusion, melatonin alleviates MASLD progression by curbing FFAs-induced oxidative stress and ferroptosis. These findings provide valuable insights into the mechanisms underlying MASLD progression and highlight melatonin as a potential therapeutic agent for the management of MASLD.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"876-889"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871265","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}

引用次数: 0

Small-Molecule-Induced Protein Polymerization: Mechanisms and Therapeutic Implications. 小分子诱导的蛋白质聚合：机制和治疗意义。

IF 3.2 3区医学

Biomolecules & Therapeutics Pub Date : 2025-09-01 Epub Date: 2025-08-12 DOI: 10.4062/biomolther.2024.211

Young-Sool Hah, Sun-Young Han

{"title":"Small-Molecule-Induced Protein Polymerization: Mechanisms and Therapeutic Implications.","authors":"Young-Sool Hah, Sun-Young Han","doi":"10.4062/biomolther.2024.211","DOIUrl":"10.4062/biomolther.2024.211","url":null,"abstract":"Small molecules that induce protein polymerization represent an emerging class of compounds with diverse therapeutic potential. This review provides a comprehensive overview of five such molecules: arsenic trioxide (As2O3), BI-3802, NVS-STG2, paclitaxel, and verteporfin. These compounds target different proteins (PML-RARα, BCL6, STING, β-tubulin, and p62, respectively) and exhibit varied mechanisms of action. Some, like As2O3 and BI-3802, induce polymerization leading to protein degradation, while others, such as NVS-STG2, activate protein function through polymerization. Paclitaxel, distinct from these, induces the stabilization of tubulin polymers. Verteporfin, on the other hand, uniquely causes covalent cross-linking of its target and other cellular proteins. This review explores the molecular mechanisms, structural insights, and therapeutic implications of these compounds, highlighting their potential in targeted protein degradation, cancer treatment, and modulation of cellular processes, such as autophagy and immune response. The diverse effects of these molecules underscore the complexity of protein polymerization in cellular function and disease, opening new avenues for drug discovery and development.","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"804-812"},"PeriodicalIF":3.2,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12408205/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144820484","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}

引用次数: 0