Biomolecules & Therapeutics最新文献

{"title":"Artificial Intelligence in Mass Spectrometry-Based Metabolomics and Lipidomics for Drug Discovery and Development.","authors":"Young Cheol Yoon, Seoyeon Choi, Cheol Woon Jung, Hendra Mahakam Putra, Young Jin Min, Sun Jo Kim, Sung Won Kwon","doi":"10.4062/biomolther.2026.225","DOIUrl":"https://doi.org/10.4062/biomolther.2026.225","url":null,"abstract":"<p><p>Artificial intelligence applied to mass spectrometry-based metabolomics and lipidomics has advanced through three technological generations: chemometric and classical machine learning, deep learning, and self-supervised foundation models, with large language models so far entering mainly at the edges. The metabolome and lipidome lie closest to drug action, yet they have been among the slowest omics layers to adopt modern artificial intelligence. This paradox arises from their downstream position, which leaves them without a closed molecular reference and without the standardized, readily modeled data available to the genome and transcriptome. This review examines what these methods contribute to drug discovery and development. We survey applications across the drug-development pipeline, from target identification and mechanism-of-action deconvolution, through the prediction of drug-induced toxicity, to pharmacometabolomics, in which pre-dose metabolic phenotypes inform patient stratification and dosing. Across these metabolomic and lipidomic applications, interpretable classical machine learning remains the dominant form of artificial intelligence. The newer deep-learning and foundation models have concentrated instead on compound annotation, the cross-cutting problem of assigning confident identities to spectra, yet successive generations have mitigated but not solved it. Beyond annotation confidence, batch effects, semi-quantification, and small-cohort overfitting also remain practical constraints. Overall, targeted, hypothesis-driven metabolomic and lipidomic studies can already support drug discovery when their inferences are restricted to confidently identified metabolites, whereas open, hypothesis-free discovery remains the frontier. Near-term progress will depend less on any single algorithm than on curated spectral resources, rigorous measurement, leakage-aware validation, and honest reporting of identification confidence.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":" ","pages":""},"PeriodicalIF":4.9,"publicationDate":"2026-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149126713","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":"Transcriptional Reprogramming of GPCR Signaling Pathways in the Frontal Cortex of Morphine Dependent Mice.","authors":"Mijin Kim, Sohyeon Moon, Taddesse Yayeh, Thea Villa, Seikwan Oh","doi":"10.4062/biomolther.2026.071","DOIUrl":"10.4062/biomolther.2026.071","url":null,"abstract":"<p><p>Repeated morphine administration for managing persistent pain frequently induces both physical and psychological dependence, accompanied by alterations in cortical gene expression. To elucidate the molecular underpinnings of morphine dependence, gene expression in the frontal cortex of mice subjected to acute and chronic morphine treatment was profiled using microarray analysis and validated by semi-quantitative PCR. Genes including <i>Drd2, Adora2a, Olfr767, Egr2, Gng7,</i> and <i>Gpr6</i> were upregulated following both acute and chronic morphine treatment. Gene ontology analysis revealed significant enrichment of differentially expressed genes in membrane components, GPCR signaling pathways, and neurological system processes, indicating integrated alterations in receptor-mediated signaling and downstream transcriptional regulation. Consistent with this, selective phosphorylation of CREB was observed during naloxone-precipitated withdrawal, highlighting CREB-dependent transcription as a key molecular correlate of cortical neuroadaptation. Behavioral assays confirmed robust physical and psychological dependence, supporting the functional relevance of these molecular changes. Collectively, these findings identify a GPCR-centered molecular framework in which coordinated regulation and functional interaction of receptors such as DRD2 and ADORA2A, along with associated signaling components, contribute to morphine-induced neuroplasticity and dependence. These insights may provide a foundation for the development of targeted therapeutic strategies to mitigate opioid dependence.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1163-1173"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534903/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863141","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":"Maslinic Acid Alleviates Obesity-Associated Skeletal Muscle Atrophy and Adipose Tissue Dysfunction in Obese Mice.","authors":"Shu-Ju Wu, Chian-Jiun Liou, Ya-Ling Chen, Hui-Ling Peng, Wen-Chung Huang","doi":"10.4062/biomolther.2026.072","DOIUrl":"10.4062/biomolther.2026.072","url":null,"abstract":"<p><p>Maslinic acid, a triterpenoid isolated from <i>Olea europaea</i> L., has been reported to exert anti-tumor and anti-inflammatory effects. Previous studies have shown that maslinic acid promotes skeletal muscle hypertrophy via mTORC1 and TGR5 signaling. Here, we examined the effects of maslinic acid on obesity-associated skeletal muscle atrophic changes and adipose tissue dysfunction. Male C57BL/6 mice were fed a high-fat diet (HFD) to induce obesity and subsequently received maslinic acid via intraperitoneal injection. In parallel, differentiated C2C12 myotubes were exposed to palmitic acid to induce lipotoxic stress-associated atrophic changes and were treated with maslinic acid to examine related cellular responses. Maslinic acid increased gastrocnemius muscle weight and attenuated obesity-associated myofiber atrophic changes in HFD-fed mice. In skeletal muscle, maslinic acid treatment was associated with increased myosin IIa expression and AKT phosphorylation, reduced expression of the atrophy-related proteins MuRF1 and Atrogin-1, and changes in mitochondrial morphology and mitochondrial dynamics-related protein expression, including increased mitofusin-2 expression and decreased phosphorylation of dynamin-related protein 1 (DRP1). Consistently, in palmitic acid-treated C2C12 myotubes, maslinic acid treatment was associated with increased myosin IIa and mitofusin-2 levels and reduced MuRF1, Atrogin-1, and DRP1 phosphorylation. In addition, maslinic acid reduced epididymal fat mass in obese mice and altered macrophage-associated marker expression in epididymal adipose tissue. Collectively, these findings suggest that maslinic acid may ameliorate obesity-associated skeletal muscle atrophic changes and adipose tissue dysfunction, accompanied by reduced adiposity and treatment-associated changes in atrophy-related, mitochondrial dynamics-related, and macrophage-associated marker expression.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1267-1280"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534901/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863644","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":"Polystyrene Nanoplastics Disrupt Immune Cell Development and Suppress T Cell Activation via mTOR and ERK Signaling.","authors":"Kang-Bin Dan, Ki-Uk Kim, Hyeyoung Min","doi":"10.4062/biomolther.2026.012","DOIUrl":"10.4062/biomolther.2026.012","url":null,"abstract":"<p><p>Plastics are globally recognized as widely used materials, but once discarded, they undergo physical and chemical decomposition, forming micro- and nano-sized particles that lead to adverse effects. Therefore, this study aimed to explore the impact of nanoplastics on immune cells and overall health. Experiments conducted with 100 nm polystyrene nanoparticles (PS-NPs) revealed a decrease in the proliferation of splenic CD4+ T cells, demonstrated by using the MTT assay, carboxyfluorescein succinimidyl ester dilution assay, Ki-67 staining, cell cycle analysis, and mTOR signaling pathway analysis. Furthermore, the differentiation of naïve CD4+ T cells into four CD4+ subsets (Th1, Th2, Th17, Treg cells) appeared to be reduced. PS-NPs were found to suppress the maturation of bone marrow-derived dendritic cells, as evidenced by a decrease in the expression of CD40, CD80, CD86, and major histocompatibility complex class II molecules, following lipopolysaccharide activation, which also reduced the division of T cells. PS-NPs interfered with the immune modulation of bone marrow-derived macrophages (BMDMs), which affected the differentiation of BMDMs into M1 or M2 macrophages. To investigate the <i>in vivo</i> effect of PS-NPs on immune cell development further, 3-week-old mice were administered water containing PS-NPs for 3 weeks. Subsequent analysis of various immune cells in the thymus, bone marrow, and spleen revealed a decrease in cell numbers in the spleen following PS-NP treatment, as well as changes in the composition of conventional dendritic cells, macrophages, and B cells. These findings suggest that PS-NPs can perturb immune cell-associated responses and homeostasis.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1255-1266"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534943/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148862827","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":"Cognitive-Enhancing Effects of Hesperetin-Rich CNE against Neuronal Damage and Memory Impairment by Regulating AKT/Nrf2 and BDNF/CREB Signaling.","authors":"Hee Ju Kim, Yeo Eun Kim, Jae Sik Yu, Gakyung Lee, Sang Suk Kim, Hyun Ok Yang","doi":"10.4062/biomolther.2026.110","DOIUrl":"10.4062/biomolther.2026.110","url":null,"abstract":"<p><p><i>Citrus nippokoreana</i>, a traditional Korean citrus species, is rich in flavonoids and polyphenols with antioxidant properties; however, its neuroprotective potential remains unclear. Neurodegeneration is closely associated with oxidative stress, neuronal apoptosis, and impaired synaptic signaling. In this study, we investigated the effects of <i>C. nippokoreana</i> peel extract (CNE, 30% ethanol) using <i>in vitro</i> and <i>in vivo</i> models. CNE significantly protected HT22 hippocampal neurons against glutamate-induced oxidative stress by reducing intracellular reactive oxygen species (ROS) and apoptosis, while regulating AKT/Nrf2-associated antioxidant pathways and enhancing BDNF/CREB signaling. In a scopolamine-induced mouse model, oral administration of CNE (50 or 100 mg/kg/day) improved cognitive performance in behavioral tests. CNE also restored the expression of BDNF, CREB, and HO-1, and reduced acetylcholinesterase activity in the hippocampus. Histological analysis confirmed reduced neuronal damage. Furthermore, serum metabolomics revealed modulation of tryptophan metabolism, phosphatidylcholine species, and redox-related pathways. To explore constituents potentially contributing to the neuroprotective effects of CNE, major compounds identified by phytochemical profiling were screened in glutamate-induced HT22 cells. Several phytochemicals exhibited protective effects, suggesting that the biological activity of CNE may result from the combined actions of multiple constituents rather than a single compound. These findings suggest that CNE attenuates oxidative stress-induced neuronal damage and improves cognitive function through coordinated regulation of antioxidant defense, neurotrophic signaling, and cholinergic function.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1174-1191"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863627","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":"Mechanistic and Clinical Perspectives on Traditional Chinese Medicine in Thyroid Cancer Management.","authors":"Yuzhuo Bai, Ke Feng, Xiaojiang Li, Xiuli Xing, Zhiyuan Zhang, Bingsen Wang, Ying Liu","doi":"10.4062/biomolther.2026.073","DOIUrl":"10.4062/biomolther.2026.073","url":null,"abstract":"<p><p>Thyroid cancer is one of the most prevalent malignancies of the endocrine system, comprising various subtypes such as papillary thyroid carcinoma (PTC), follicular thyroid carcinoma (FTC), medullary thyroid carcinoma (MTC), and the aggressive anaplastic thyroid carcinoma (ATC). Despite a generally favorable prognosis for PTC, recurrence, metastasis, and resistance to conventional therapies continue to pose significant challenges. The pathogenesis of thyroid cancer involves genetic mutations in BRAF, RAS, and RET, as well as dysregulated molecular pathways such as MAPK, PI3K/Akt/mTOR, and NF-κB, all of which contribute to cancer progression and therapeutic resistance. This review highlights how Traditional Chinese Medicine (TCM), with its extensive history and a diverse range of bioactive compounds derived from natural sources, offers a complementary approach to thyroid cancer treatment. TCM has been shown to modulate various cellular mechanisms, including inhibiting tumor proliferation, inducing apoptosis, and regulating immune responses. Additionally, TCM can influence the tumor microenvironment (TME), reducing immune evasion and improving therapeutic sensitivity. Many TCM compounds have been identified for their ability to target critical oncogenic signaling pathways, offering a holistic approach to cancer treatment with fewer side effects than traditional chemotherapy. Furthermore, integrating TCM with modern medicine, including novel formulations and nanotechnology, offers the potential to improve efficacy and reduce side effects. The convergence of Artificial Intelligence (AI) and Systems Biology also holds great promise for optimizing personalized treatment regimens and advancing targeted therapies, ultimately improving patient outcomes in thyroid cancer management.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1119-1135"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534908/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863611","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":"Epigenetic Repression of <i>TP53</i> Transcription Underlies Cancer Cell Persistence for Carboplatin Resistance in Non-Small Cell Lung Cancer.","authors":"Sojung Ha, Woo-Young Kim","doi":"10.4062/biomolther.2026.158","DOIUrl":"10.4062/biomolther.2026.158","url":null,"abstract":"<p><p>While chemoresistance in non-small cell lung cancer (NSCLC) cells has historically been attributed to permanent genetic mutations, emerging evidence highlights the role of nongenetic transcriptional plasticity and 'drug-tolerant persister' cells. To systematically map these epigenetic vulnerabilities, we utilized a genome-wide CRISPR interference library to screen wild-type <i>TP53</i> NSCLC (A549) cells under carboplatin selection. Using the DrugZ algorithm and subsequent pathway enrichment analyses, this screen revealed that transcriptional suppression of interstrand crosslink DNA repair networks, including the Fanconi anemia pathway, markedly sensitized cells to carboplatin. Unexpectedly, transcriptional silencing of <i>TP53</i> and its downstream target <i>CDKN1A</i> emerged as the strongest drivers of resistance, enabling cells to bypass therapy-induced senescence and maintain their proliferative potential later. To validate these findings in a clinically relevant context, we established a chronic carboplatin-resistant cell model (A549Carbo^R cells). A549Carbo^R exhibited a reduction in <i>TP53</i> transcripts, along with decreased H3K27 acetylation and increased DNA hypermethylation on its promoter. Epigenetic remodeling using the DNA methyltransferase inhibitor (DNMTi) was associated with unblocking <i>TP53</i> transcription, restored p53 signaling, and resensitization of resistant cells to carboplatin. Conversely, histone deacetylase inhibitors induced <i>CDKN1A</i> transcription to bypass <i>TP53</i>, indicating distinct epigenetic circuits. Collectively, the results demonstrate for the first time that <i>TP53</i> expression is dynamically regulated at the transcriptional level through promoter methylation related to the drug tolerance. These insights emphasize that epigenetic silencing, rather than exclusive genetic loss-of-function, contribute to platinum resistance and underscore the therapeutic potential of pairing platinum regimens with DNMTi to target the transcriptomic plasticity of persistent cancer cell populations.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1221-1231"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863613","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":"Epigenetic Silencing of miR-124 Drives KITENIN Activation in Colorectal Cancer.","authors":"So-Yeon Park, Mücahit Varlı, Hangun Kim","doi":"10.4062/biomolther.2026.020","DOIUrl":"10.4062/biomolther.2026.020","url":null,"abstract":"<p><p>Aberrant epigenetic regulation of microRNAs and their targets contributes to colorectal cancer (CRC) progression. This study examined the methylation-dependent regulation of the miR-124-KITENIN axis and its clinical significance in CRC. Site‑specific hypermethylation within the KITENIN (VANGL1) locus, particularly at cg00819310, was associated with poorer patient survival. miR-124, a direct negative regulator of KITENIN, was frequently hypermethylated and transcriptionally silenced, leading to KITENIN upregulation. Treatment with 5-aza-2'-deoxycytidine restored miR-124 expression and reduced KITENIN levels in CRC cells. These results demonstrate that miR-124 silencing enhances KITENIN activation and CRC progression, supporting miR-124 methylation as a potential prognostic and therapeutic target.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1207-1220"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534898/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863615","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":"Erratum to \"Interleukin-1β Signaling Contributes to Cell Cycle Arrest and Apoptotic Cell Death by Leptin via Modulation of AKT and p38MAPK in Hepatocytes\" [Biomol Ther 32(5), 611-626 (2024)].","authors":"Ananda Baral, Pil-Hoon Park","doi":"10.4062/biomolther.2026.011","DOIUrl":"10.4062/biomolther.2026.011","url":null,"abstract":"","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1281"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534983/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148863601","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":"Single-Cell Transcriptomics of Pyrimidine Salvage in HBV-Related HCC Reveals Prognostic and Immune Infiltration Features.","authors":"Liping Xie, Shaoyang Wang, Taofa Lin","doi":"10.4062/biomolther.2025.223","DOIUrl":"10.4062/biomolther.2025.223","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is primarily caused by hepatitis B virus (HBV). The pyrimidine-salvage pathway (PSP) is crucial for tumor proliferation, but its prognostic and immunomodulatory roles in HBV-HCC are unclear. By using single-cell transcriptomics, we investigated PSP signatures and their link to clinical outcomes and immune modulation in HBV-HCC. Data from XENA and GEO databases were analyzed. Malignant cell subpopulations were identified, and single-cell PSP activity was quantified. HBV-specific malignant subpopulations were characterized using the Ro/e metric. Cell-cell communication was analyzed. A prognostic model was developed and validated using a training cohort, and a nomogram was constructed. Immune infiltration, drug sensitivity, and the functional role of ferritin light chain (FTL) were examined experimentally. Malignant cells were classified into HBV⁻ and HBV⁺ subpopulations. The HBV⁺ group showed low PSP gene (PSPG) expression. The six-gene prognostic model demonstrated high predictive accuracy for 1-, 3-, and 5-year survival. High-risk patients had shorter survival and increased infiltration of macrophages, Tregs, and activated dendritic cells. Drug sensitivity analysis identified potential agents. <i>In vitro</i>, FTL silencing suppressed HBV-HCC cell proliferation and migration. This investigation clarified the prognostic significance of PSPGs and their immunomodulatory roles in HBV-HCC, and established a prognostic model with predictive power. FTL, identified as a key gene, represented a potential therapeutic target for HBV-HCC. These findings provided a novel theoretical foundation for the treatment of HBV-HCC.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 5","pages":"1232-1254"},"PeriodicalIF":4.9,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13534984/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148862976","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}