Biomolecules & Therapeutics最新文献

{"title":"γ-Elemene Impairs Mitochondrial Biogenesis in Breast Cancer Cells by Upregulating GCN5-Mediated PGC-1α Acetylation.","authors":"Ling Tang, Mingyan Wang, Jia Liu, Qiong Yu, Chen Chen, Lihua Jia, Jiyi Xia","doi":"10.4062/biomolther.2025.119","DOIUrl":"10.4062/biomolther.2025.119","url":null,"abstract":"<p><p>Mitochondrial biogenesis represents a promising therapeutic target in triple-negative breast cancer (TNBC) due to its essential role in cancer cell metabolism and survival. The natural compound γ-Elemene exhibits potent anti-tumor activity, but its effects on mitochondrial regulation in TNBC remain unclear. In this study, we demonstrate that γ-Elemene induces dose-dependent cytotoxicity in MDA-MB-468 and HCC1806 TNBC cells while significantly impairing mitochondrial function, as shown by reduced membrane potential, oxidative phosphorylation capacity, and ATP production. γ-Elemene treatment markedly suppressed mitochondrial biogenesis, decreasing mitochondrial DNA content and downregulating key mitochondrial genes and proteins. These effects were associated with reduced expression of the master regulators NRF1 and TFAM, but independent of PGC-1α expression levels. Mechanistically, γ-Elemene upregulated the acetyltransferase GCN5, leading to enhanced PGC-1α acetylation. This upregulation occurs primarily through increased GCN5 transcription. Genetic ablation of GCN5 completely reversed γ-Elemene-induced PGC-1α acetylation and restored mitochondrial biogenesis and cell viability, establishing a critical role for GCN5 in mediating these effects. Our findings reveal a novel mechanism whereby γ-Elemene disrupts mitochondrial function in TNBC through GCN5-mediated PGC-1α acetylation, providing new insights into its anti-cancer properties and potential therapeutic applications against TNBC.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"165-173"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782864/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145653527","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":"Targeting Ferroptosis to Overcome Drug Resistance in Cancer: Molecular Mechanisms and Therapeutic Prospects.","authors":"Sang Hoon Joo, Yong-Yeon Cho, Jung-Hyun Shim","doi":"10.4062/biomolther.2025.211","DOIUrl":"10.4062/biomolther.2025.211","url":null,"abstract":"<p><p>Drug resistance in cancer cells remains a major obstacle limiting the clinical efficacy of current anticancer therapies. The induction of ferroptosis, an iron-dependent, regulated form of cell death, may offer an alternative therapeutic strategy to overcome such resistance. The generation of reactive oxygen species (ROS) has been implicated in this process, and depending on the cellular context, ROS can be either detrimental or beneficial. Ferroptosis can be effectively triggered in drug-resistant cancer cells in which ROS levels are often highly elevated. Key signaling pathways, including receptor tyrosine kinase (RTK), mitogen-activated protein kinase (MAPK), and nuclear factor erythroid 2-related factor 2 (NRF2), are promising targets for modulating ROS homeostasis and sensitizing cancer cells to ferroptosis. In this review, we discuss the molecular mechanisms governing ferroptosis, the interplay between ROS and ferroptosis resistance, and emerging therapeutic approaches designed to enhance ferroptosis induction in drug-resistant cancer cells. Altogether, a combination of ferroptosis inducers and conventional treatments may improve the therapeutic efficacy and help overcome resistance mechanisms.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 1","pages":"18-29"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782861/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145905772","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":"Adaptive Immunity and Alzheimer's Disease: Dual Roles in Neurodegeneration and Neuroprotection with Therapeutic Implications.","authors":"You Min Ahn, Min-Kyoo Shin","doi":"10.4062/biomolther.2025.199","DOIUrl":"10.4062/biomolther.2025.199","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is a progressive neurodegenerative disorder defined by amyloid-β (Aβ) plaques, tau hyperphosphorylation, and neuroinflammation. Although earlier work emphasized brain-resident glia (microglia and astrocytes), recent studies highlight adaptive immune cells, particularly T and B lymphocytes, as modulators of AD pathology. This review synthesizes animal and human findings from 2022-2025 to provide updated insights into the multifaceted roles and therapeutic potential of adaptive immunity in AD. Infiltration of peripheral T and B cells into the brain parenchyma links peripheral immunity to central nervous system (CNS) pathology. Both infiltrating lymphocytes and resident glia show context-dependent dual effects, either exacerbating neurodegeneration or promoting neuroprotection. Therapeutic strategies under active investigation include modulation of CD4⁺ T cell differentiation, adoptive transfer of regulatory T cells, and next-generation active vaccines for AD. Overall, selective modulation of discrete immune subsets may enable adaptive-immunity-based treatments, a complex yet promising avenue for AD therapy.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 1","pages":"124-135"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782867/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145905604","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":"Chrysoeriol Exerts Antiplatelet Effects by Regulating cAMP/cGMP and PI3K/MAPK Pathway.","authors":"Ga Hee Lee, Jin Pyo Lee, Akram Abdul Wahab, Na Yoon Heo, Chang Eun Park, Dong-Ha Lee","doi":"10.4062/biomolther.2025.090","DOIUrl":"10.4062/biomolther.2025.090","url":null,"abstract":"<p><p>Chrysoeriol, a flavonoid naturally found in several plants, including Danggui Susan, a traditional herbal medicine, exhibits promising anti-inflammatory and antioxidant properties. Its potential to prevent cardiovascular diseases, primarily through inhibiting platelet activation and aggregation, has attracted significant interest. This study aimed to investigate the molecular mechanisms underlying the antiplatelet effects of chrysoeriol. The compound effectively suppressed collagen-induced platelet aggregation without inducing cytotoxicity. Chrysoeriol elevated intracellular levels of cyclic AMP (cAMP) and cyclic GMP (cGMP), enhanced inositol 1,4,5-trisphosphate receptor (IP₃R) phosphorylation, and reduced cytosolic calcium (Ca²⁺) mobilization, all of which contributed to its antiplatelet action. Furthermore, chrysoeriol inhibited the phosphorylation of PI3K, Akt, JNK, and p38 MAPK, pathways involved in the activation of cytosolic phospholipase A2 (cPLA₂) and thromboxane A2 (TXA₂) production. These effects were accompanied by reduced TXA₂ production and secretion of dense granules (ATP and serotonin). Chrysoeriol also impaired thrombin-induced clot retraction, further suggesting its capacity to regulate platelet responses and cytoskeletal rearrangements. These findings highlight chrysoeriol's multi-target mechanisms, including modulation of cyclic nucleotides, kinase pathways, and platelet function, offering potential as a therapeutic agent to prevent thrombotic cardiovascular events.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"202-212"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782860/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145653380","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":"Targeting YAP-TEAD Interaction with Honokiol to Inhibit Melanoma Progression and Metastasis.","authors":"Chaelin Lee, Hien Thi Thu Do, Xiang Fei, Sanha Lee, Soonsil Hyun, Seung-Yong Seo, Inmoo Rhee","doi":"10.4062/biomolther.2025.224","DOIUrl":"10.4062/biomolther.2025.224","url":null,"abstract":"<p><p>The Hippo-YAP/TEAD pathway plays a central role in melanoma progression by regulating tumor cell proliferation, survival, and migration. Using a NanoLuc Binary Technology (NanoBiT) protein-protein interaction assay, we screened honokiol-based small molecules and identified several analogues that disrupt the YAP-TEAD interaction. HK03 was the most effective analogue, leading to a pronounced reduction in Cyr61 levels and diminished Erk and Akt phosphorylation in B16-F10 melanoma cells. HK03 also blocked epithelial-mesenchymal transition (EMT) and impaired melanoma cell migration in wound-healing assays. <i>In vivo</i>, HK03 treatment markedly reduced metastatic burden in a B16-F10 lung metastasis model. These findings suggest that honokiol derivatives, particularly HK03, represent potential lead compounds for targeting the YAP-TEAD axis in melanoma therapy.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"154-164"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782857/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802978","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":"β-Catenin and AMPK/AKT/FOXO Signaling Mediate Doxorubicin-Induced Senescence and Lipid Accumulation in C2C12 Myoblasts.","authors":"Chawon Yun, Sou Hyun Kim, Doyoung Kwon, RanJu Woo, Ki Wung Chung, Jaewon Lee, Yun-Hee Lee, Young-Suk Jung","doi":"10.4062/biomolther.2025.217","DOIUrl":"10.4062/biomolther.2025.217","url":null,"abstract":"<p><p>Skeletal muscle atrophy is a major complication associated with aging, chronic disease, and chemotherapy. Doxorubicin (Dox), a widely used anticancer agent, accelerates muscle wasting; however, the underlying cellular mechanisms remain poorly understood. In this study, we examined the effects of Dox on myogenic differentiation, senescence, and lipid metabolism using C2C12 myoblasts. Dox exposure impaired myotube formation without causing overt cytotoxicity. Mechanistically, Dox disrupted myogenic differentiation by inhibiting protein kinase B/mammalian target of rapamycin (AKT/mTOR) signaling, thereby de-repressing forkhead box O1/3 (FOXO1/3) and upregulating the muscle-specific ubiquitin ligases muscle atrophy F-box (MAFbx) and muscle RING finger 1 (MuRF1), which promote proteolysis. Dox also decreased glycogen synthase kinase 3β (GSK3β) phosphorylation while paradoxically increasing total and phosphorylated β-catenin, indicating dysregulated Wnt/β-catenin signaling. These alterations were accompanied by a senescence-like phenotype, characterized by elevated senescence-associated β-galactosidase (SA-β-gal) activity, increased phosphorylated histone variant γH2AX, and activation of the p53-p21 axis. Notably, cellular senescence coincided with excessive lipid accumulation in myotubes. Dox reduced phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) while enhancing expression of key lipogenic regulators, thereby creating a metabolic environment favoring lipid storage. Collectively, these findings demonstrate that Dox not only suppresses myogenic differentiation but also induces premature senescence and metabolic reprogramming toward lipid accumulation. Targeting these pathways through AMPK activation, FOXO inhibition, or senolytic interventions may offer therapeutic strategies to preserve skeletal muscle integrity in patients undergoing chemotherapy.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"136-145"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782858/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145780169","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":"Gene Editing of Pluripotent Stem Cell-Derived Hepatic Cells for Liver Disease Modeling and Therapeutic Development.","authors":"Donghyun Lim, Hyung-Ryong Kim","doi":"10.4062/biomolther.2025.239","DOIUrl":"10.4062/biomolther.2025.239","url":null,"abstract":"<p><p>The growing demand for physiologically relevant human liver models has driven significant progress in generating hepatic cells and organoids derived from pluripotent stem cells. These regenerative cell sources serve as powerful platforms for elucidating the mechanisms underlying liver diseases and for evaluating drug responses under human-relevant conditions. Moreover, they hold tremendous promise as cell-based therapeutics for various hepatic disorders. The utility of these regenerative cell technologies is further expanded when combined with gene-editing techniques, which enable precise modeling of pathogenic variants and targeted correction of disease-associated mutations. Gene editing can also be leveraged to enhance the functionality and therapeutic potential of regenerative hepatocyte products. In this review, we summarize recent advances at the interface of gene editing and hepatic cell regeneration, emphasizing their applications in genetic disease modeling, therapeutic gene correction, drug testing, and cell-based therapies for liver disorders. We also provide an overview of major gene-editing tools and practical guidance for implementing them in pluripotent stem cells-based regenerative workflows, concluding with future perspectives on the integration of gene editing and regenerative hepatocyte technologies.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"102-123"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782869/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145802926","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":"Navigating the New Therapeutic Landscape: Innovative Strategies for Overcoming Resistance and Degeneration.","authors":"Hyun-Jeong Ko, Chang Hoon Lee","doi":"10.4062/biomolther.2025.008","DOIUrl":"10.4062/biomolther.2025.008","url":null,"abstract":"<p><p>Recent technological advancements and environmental shifts have reshaped the therapeutic landscape of human diseases, driving a transition from merely understanding pathogenesis to developing precise and targeted therapeutic solutions. While the 2025 Special Issue focused on identifying emerging risk factors, the 2026 Special Issue (Vol. 34, No. 1) pivots toward concrete methodological innovations and advanced therapeutic interventions. This issue presents a curated collection of ten distinguished articles organized around three core themes. First, in the field of oncology and drug resistance, studies investigate transglutaminase 2 (TG2)-mediated autophagy and ferroptosis as strategies to overcome therapeutic resistance, alongside advances in CAR-T cell engineering and the integration of artificial intelligence (AI) with robotic surgery to enable precision medicine. Second, addressing degenerative and metabolic diseases, contributions elucidate the role of Wnt/β-catenin signaling in osteoporosis, recent therapeutic advances in knee osteoarthritis, mechanisms underlying drug-induced senescence, and the application of gene-editing technologies in iPSC-derived hepatic models. Finally, investigations into the neuro-immune axis highlight the dual roles of adaptive immunity in Alzheimer's disease and evaluate novel pharmacological modulators targeting the kynurenine-aryl hydrocarbon receptor (AhR) axis. Collectively, this Special Issue delivers groundbreaking insights and innovative strategies aimed at restoring biological homeostasis and overcoming intractable diseases.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 1","pages":"1-5"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782856/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145905654","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":"Curzerene Ameliorates Depression-Like Behaviors and Cognitive Impairment by Modulating the Gut Microbiota and HMGB1/RAGE/TLR4 Pathway.","authors":"Fengjing Huang, Xiaohong Ma, Xiao Xu, Jingwen Zhang, Chunlai Wang, Ruoxi Song, Xiangxiang Wang, Mingxing Chen, Yu Qi","doi":"10.4062/biomolther.2025.120","DOIUrl":"10.4062/biomolther.2025.120","url":null,"abstract":"<p><p>Curzerene, a sesquiterpene compound isolated from Curcuma Radix, exhibits various therapeutic effects, such as anti-tumor and anti-hyperlipidemic properties. However, its neuroprotective effects have not yet been reported. This study focused on exploring the neuroprotective effect of curzerene and elucidating its potential mechanism by combining molecular biotechnology with multi-omics approaches. Curzerene was orally administered to LPS-induced depressive-like behaviors and cognitive impairment in mice for 14 days, and the related biochemical parameters were evaluated. The possible mechanisms were elucidated using qRT-PCR, Western Blot, immunofluorescence, untargeted metabolomics, GC-MS and 16S rDNA comprehensively. Curzerene ameliorated depression symptoms and cognitive impairment by increasing the preference for sucrose in SPT and the central area and total distance traveled in OFT, reducing the immobility time in TST and FST, as well as rising the spontaneous alternation ratio in Y maze. Multiple molecular biology techniques analyses indicated the ameliorative effect of curzerene via HMGB1/RAGE/TLR4 pathway. Moreover, curzerene primarily regulates purine metabolism, phenylalanine, tyrosine and tryptophan biosynthesis, phenylalanine metabolism, pyrimidine metabolism, etc. Furthermore, intervention increased the relative abundance of <i>Parabacteroides, Clostridia_UCG-014_unclassified</i>, and <i>Rhodospirillales_unclassified</i>, and enhanced the production of SCFAs. This work demonstrated that curzerene effectively protects against LPS-induced neurological damage, potentially by inhibiting the HMGB1/RAGE/TLR4 pathway through the restoration of gut microbiota homeostasis, modulation of metabolites, and enhancement of SCFAs. In conclusion, this study offers new perspectives on the therapeutic possibilities of curzerene in mitigating depressive-like behaviors and cognitive impairment.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"174-188"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782868/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720760","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":"Integrating Robotic Bilateral Axillo-Breast Approach Thyroidectomy with Molecular Diagnostics and Artificial Intelligence in Thyroid Cancer Care.","authors":"Qiang Deng, Xiaoping Men, Duo Jin, Yuzhuo Bai","doi":"10.4062/biomolther.2025.125","DOIUrl":"10.4062/biomolther.2025.125","url":null,"abstract":"<p><p>Thyroid cancer is one of the most prevalent cancers in the world, accounting for the increased sensitivity of diagnostic assessments, the environment, and extensive imaging. While open thyroidectomy still forms the base surgical treatment of differentiated thyroid carcinoma (DTC), its visible scarring and postoperative morbidity have mandatorily propelled a longitudinal shift to minimally invasive techniques. Robotic thyroidectomy using the bilateral axillo-breast approach (BABA) is an emerging transformative technique that combines robotic precision and visualization with oncologic efficacy and superior cosmetic outcomes to enhance recovery. Molecular diagnostics such as next-generation sequencing (NGS) and microRNA classifiers have transformed preoperative planning. These tools aid in accurate risk stratification, enabling clinicians to determine the course of surgery and avoid overtreatment. Artificial intelligence (AI) enhances precision medicine by improving nodule classification, predicting surgical risks, providing intraoperative navigation guidance, and supporting postoperative histopathological evaluations. Despite these innovations, cost, accessibility, and ethical governance issues highlight persistent challenges. This review consolidates the current state of robotic-assisted surgery for thyroid cancer with molecular profiling and AI. It proposes future aims and strides toward precision surgery that is accessible worldwide.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":"45-64"},"PeriodicalIF":3.2,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12782870/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145720787","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}