Biomolecules & Therapeutics最新文献

{"title":"Pseudoephedrine Improves Chronic Obstructive Pulmonary Disease by Regulating Airway Senescence and Mitochondrial Function through PI3K/AKT/mTOR Axis.","authors":"Lijuan Wu, Fenqiao Chen, He Zhang, Wenzhong Xu, Tan'e Liu, Ming Liu, Lianxing Liu, Jianqiang Mei","doi":"10.4062/biomolther.2025.190","DOIUrl":"10.4062/biomolther.2025.190","url":null,"abstract":"<p><p>Ephedra can improve chronic obstructive pulmonary disease (COPD). Pseudoephedrine (PSE) is a main active ingredients of ephedra. It has anti-inflammatory pharmacological properties. Its effect on COPD and its possible mechanism have not been elucidated. The COPD rat model was constructed by systemic cigarette smoke exposure combined with lipopolysaccharide (LPS) tracheal instillation. BEAS-2B cells were treated using cigarette smoke extract; PSE was administered for treatment. The senescence level of rat lung tissue and bronchial epithelial cells was evaluated through staining, immunofluorescence and western blot. The mitochondrial damage of rats and BEAS-2B cells was detected by transmission electron microscopy, JC-1 probe, MitoSOX Red probe and kits. In addition, the lung function indexes of rats were detected by animal lung function analysis system. Hematoxylin and eosin (HE) staining analyzed the pathological damage. Enzyme-linked immunosorbent assay (ELISA), kit and immunohistochemistry were used to evaluate inflammation and oxidative stress. Western blot detected phosphoinositide 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/AKT/mTOR) axis protein. PSE significantly reduced senescent cells, apoptosis rate and P21 level in rat lung tissue and BEAS-2B cells, significantly increased the levels of zonula occludens-1 (ZO-1)and adenosine triphosphate (ATP), restored mitochondrial structure, and visible mitochondrial cristae. It also inhibited reactive oxygen species (ROS) levels and mitochondrial excessive fission. PSE also significantly improved lung function in rats, increased mean alveolar number (MAN), reduced pro-inflammatory factors, and increased superoxide dismutase (SOD) levels. PSE markedly suppressed p-p85, p-AKT and p-mTOR protein expressions. In addition, the PI3K/AKT agonist 740Y-P weakened the effect of PSE on improving COPD. PSE inhibited PI3K/AKT/mTOR axis, improved lung tissue senescence, mitochondrial dysfunction and pathological damage, and reduced airway inflammation and oxidative stress damage, thereby alleviating COPD.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"589-607"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761223","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":"FDFT1 Acts as a Negative Regulator of Autophagy by Modulating AMPK-ULK1 Signaling in Hepatocellular Carcinoma Cells.","authors":"Thi Ha Nguyen, Yongook Lee, Minh Tuan Nguyen, Seoung Gyu Choi, Phuong Ngan Nguyen, Boram Kim, Eun Ji Kim, Gyeoung Jin Kang, Mi Kyung Park, Sung Hoon Lee, Sang Geon Kim, Chang Hoon Lee","doi":"10.4062/biomolther.2025.178","DOIUrl":"10.4062/biomolther.2025.178","url":null,"abstract":"<p><p>Autophagy is a conserved catabolic process that degrades proteins and damaged organelles to maintain cellular homeostasis, and its role in cancer depends on stage and context. Farnesyl-diphosphate farnesyltransferase 1 (FDFT1) is an essential enzyme in the sterol branch of the mevalonate pathway, but its functions in hepatocellular carcinoma (HCC) and in the regulation of autophagy remain poorly understood. In this study, we show that FDFT1 acts as a negative regulator of autophagy in HCC cells. Loss of FDFT1 led to increased autophagosome formation and fusion with lysosomes, whereas its overexpression suppressed both basal and induced autophagy. These changes were associated with AMPK-ULK1 signaling, suggesting that FDFT1 influences a central pathway controlling autophagy. Our findings connect cholesterol metabolism with autophagy regulation and tumor growth, highlighting FDFT1 as a potential prognostic marker and therapeutic target in liver cancer.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"632-640"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149159/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761134","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":"The RIPK3 Inhibitor GSK872 Attenuates Inflammation and Necroptosis via Modulation of the JNK Signaling Pathway in LPS-Stimulated Microglia.","authors":"Jin-Sun Park, Do-Yeon Kim, Seong-Eun Kim, Jin-Won Hyun, Hee-Sun Kim","doi":"10.4062/biomolther.2025.208","DOIUrl":"10.4062/biomolther.2025.208","url":null,"abstract":"<p><p>Microglia are the resident immune cells of the brain; they respond rapidly to inflammatory stimuli and contribute to the progression of neurodegenerative diseases. Receptor-interacting protein kinase 3 (RIPK3) is known to mediate pro-inflammatory signaling and necroptosis, a form of regulated necrotic cell death. However, the role of RIPK3 in microglial activation remains unclear. This study aimed to investigate the role of RIPK3 in both in vitro and in vivo models of neuroinflammation and necroptosis using a selective RIPK3 inhibitor, GSK872. In lipopolysaccharide (LPS)-injected mice, GSK872 attenuated microglial activation, decreased the expression of pro-inflammatory mediators, and reduced the phosphorylation of RIPK3 and mixed lineage kinase domain-like protein (MLKL). In BV2 microglial cells, GSK872 suppressed the production of inflammatory mediators under both inflammatory and necroptotic conditions induced by LPS or LPS/Z-VAD. In particular, GSK872 reduced necroptosis-associated cell death and the release of HMGB1 and IL-1β in LPS/Z-VAD-treated cells. Detailed mechanistic studies revealed that GSK872 inhibits the c-Jun N-terminal kinase (JNK) pathway, while pharmacological inhibition of JNK using SP600125 recapitulates the effects of GSK872 on inflammatory and necroptotic markers. These results indicate that JNK plays a critical role in mediating the effects of GSK872. Notably, IL-1β released during necroptosis appears to contribute modestly to the phosphorylation of JNK and MLKL, indicating a potential feedback mechanism that reinforces necroptotic signaling. Our findings provide compelling evidence that the inhibition of RIPK3 by GSK872 alleviates neuroinflammatory responses and necroptotic cell death by modulating JNK signaling in activated microglia, offering a promising therapeutic strategy for neurodegenerative diseases.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"565-577"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149048/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761216","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 \"Hemostasis-Sparing Antiplatelet Therapy: Current Concepts and Emerging Targets in Arterial Thrombosis\" [Biomol Ther 34(2), 225-237 (2026)].","authors":"Ji Won Park, Eun Bee Oh, Tong-Shin Chang","doi":"10.4062/biomolther.2026.006","DOIUrl":"10.4062/biomolther.2026.006","url":null,"abstract":"","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"722"},"PeriodicalIF":3.2,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149052/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761094","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":"α-MSH Induces Intracellular ROS Generation in Melanoma Cells through NADPH Oxidase-1/4 Activation.","authors":"Kyuri Kim, Jihyun Yoon, Hye Yeon Kim, Kyung-Min Lim","doi":"10.4062/biomolther.2025.258","DOIUrl":"10.4062/biomolther.2025.258","url":null,"abstract":"<p><p>α-Melanocyte-stimulating hormone (α-MSH) is a key physiological inducer of melanogenesis and melanocyte activation. Reactive oxygen species (ROS) function as secondary messengers in intracellular signaling pathways that regulate α-MSH-mediated melanogenesis. However, the mechanism by which α-MSH induces ROS generation in melanocytes remains incompletely understood. Here, we investigated the sources and regulatory mechanisms of α-MSH-induced ROS in murine B16F10 and human MNT-1 melanoma cells. Confocal microscopy revealed that α-MSH predominantly stimulated cytosolic rather than mitochondrial ROS generation. Western blot analysis showed that α-MSH upregulated the expression of NADPH oxidases NOX1 and NOX4 at early time points, key enzymes involved in cytosolic ROS production. Pharmacological inhibition of NOX1/4 significantly reduced α-MSH-induced ROS levels and melanin content, accompanied by decreased phosphorylation of MITF, a melanogenic transcription factor. These findings indicate that α-MSH is a key physiological inducer of melanogenesis and melanocyte-related signaling in melanoma cells. Our study highlights NOX4, together with NOX1, as potential targets for anti-pigmentation strategies.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"709-721"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149053/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761246","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":"Combination Therapy with Betulinic Acid and TRAIL Increases ROS-Dependent Cytotoxicity and Inhibits PI3K/Akt Signaling in Human Bladder Cancer Cells.","authors":"Cheol Park, Hee-Jae Cha, Su Hyun Hong, Heui-Soo Kim, Sun-Hee Leem, Jung-Hyun Shim, Gi-Young Kim, Kyoung Ah Kang, Jin Won Hyun, Yung Hyun Choi","doi":"10.4062/biomolther.2026.035","DOIUrl":"10.4062/biomolther.2026.035","url":null,"abstract":"<p><p>Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a cytokine that selectively targets cancer cells and induces apoptosis. However, many cancers, including bladder cancer, develop resistance to TRAIL, limiting the efficacy of TRAIL-based therapies. This study investigated whether betulinic acid (BA), a pentacyclic triterpenoid with anticancer and chemosensitizing properties, increases TRAIL-mediated apoptosis in TRAIL-resistant human bladder cancer cells. Combination treatment with BA and TRAIL significantly increased cytotoxicity and apoptosis compared to either treatment alone. This combination treatment also increased reactive oxygen species (ROS) production, increased Bax expression and Bid cleavage (tBid formation), and downregulated Bcl-2 levels. These effects were accompanied by caspase activation via extrinsic and intrinsic pathways, leading to cytochrome c release via mitochondrial membrane destabilization, thereby contributing to increased apoptosis. Furthermore, the combination treatment inhibited phosphoinositide 3-kinase (PI3K) and Akt phosphorylation; this effect was amplified by a PI3K inhibitor but abrogated by ROS inhibition. Collectively, our results suggest that BA sensitizes bladder cancer cells to TRAIL-induced apoptosis via ROS-dependent activation of the apoptotic pathway and inhibition of PI3K/Akt signaling. Therefore, the BA and TRAIL combination exhibits potential to overcome TRAIL resistance in human bladder cancer.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"641-651"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149091/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761115","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":"Zoledronic Acid Inhibits the Growth of ER-Positive Breast Cancer Cells by Inducing Ferroptosis.","authors":"Shaofei Yuan, Dejin Shi, Yiyin Xu, Tao Wu, Shuifeng Liang, Dinghao Chen, Jiayi Wang, Guang Wu, Jiawei Cao","doi":"10.4062/biomolther.2025.132","DOIUrl":"10.4062/biomolther.2025.132","url":null,"abstract":"<p><p>Zoledronic acid (ZA), a nitrogen-containing bisphosphonate with established clinical utility in osteoporosis management, exhibits emerging antitumor potential in estrogen receptor-positive breast cancer. However, the molecular mechanisms underlying its non-apoptotic anticancer effects remain poorly characterized. This study revealed that ZA induced ferroptosis in ER+ breast cancer cells through dual suppression of cystine-glutamate antiporter SLC7A11 and glutathione peroxidase 4 (GPX4), key repressors of ferroptosis. Pharmacological inhibition of ferroptosis using Ferrostatin-1 significantly attenuated ZA-induced cytotoxicity, while combinatorial treatment with the GPX4 inhibitor RSL3 synergistically enhanced lipid peroxidation and cell death. Mechanistically, ZA activated the Hippo-YAP signaling pathway, promoting YAP phosphorylation, proteasomal degradation, and cytoplasmic retention, thereby silencing SLC7A11 and GPX4. We established a novel metabolic vulnerability in hormone-responsive malignancies. These findings position ZA as a bifunctional ferroptosis inducer in ER+ breast cancer, offering a promising strategy to overcome endocrine resistance.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"608-617"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149051/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761214","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":"RBM15-Mediated m6A Modification Regulates Proliferation and Migration of Pancreatic Cancer Cells via the lncRNA LINC01320/miR-1287-5p/FBXO11 Axis.","authors":"Xin Deng, Baosheng Wang","doi":"10.4062/biomolther.2025.159","DOIUrl":"10.4062/biomolther.2025.159","url":null,"abstract":"<p><p>Pancreatic cancer (PC) is life-threatening with unfavorable outcomes. RBM15, an m6A methylation modulator, is a potential biomarker for cancers. This study delved into the mechanism of RBM15-mediated m6A modification in PC. RBM15, LINC01320, miR-1287-5p, and FBXO11 levels in PC tissues and cells were examined. Cell proliferation, invasion, and migration were determined. The enrichment of m6A on LINC01320 and LINC01320 stability were detected. Joint experiments were designed to analyze the role of LINC01320 or FBXO11 in PC cell growth. The tumor xenograft in nude mice was established, and the effect of RBM15 on PC cell proliferation was verified in vivo. RBM15, LINC01320, and FBXO11 were significantly increased in PC, while miR-1287-5p was decreased. RBM15 downregulation reduced PC cell proliferation, invasion, and migration. In mechanism, RBM15-mediated m6A modification increased LINC01320 stability and its expression, thus upregulating FBXO11 transcription by competitively binding to miR-1287-5p. Overexpression of LINC01320 or FBXO11 abated the inhibition of RBM15 downregulation on PC cells. RBM15 knockdown inhibited tumor size and weight and reduced the positive rate of Ki67 through LINC01320/miR-1287-5p/FBXO11 axis. Overall, RBM15-mediated m6A modification increases LINC01320 stability and promotes its expression and FBXO11 transcription by competitive binding to miR-1287-5p, ultimately promoting PC cell growth.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"618-631"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149094/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761191","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":"Developmental Exposure to Endocrine Disruptors and Persistent Pollutants Heightens Addiction Risk via Toxicological Mechanisms.","authors":"Se Jin Jeon, Dae Hyun Kim, Chan Young Shin","doi":"10.4062/biomolther.2025.234","DOIUrl":"10.4062/biomolther.2025.234","url":null,"abstract":"<p><p>Endocrine-disrupting chemicals (EDCs) and persistent organic pollutants (POPs) cross the placenta and accumulate during gestation and early postnatal life, periods of heightened hormonal and neurodevelopmental plasticity. Exposure to contaminants such as bisphenol A (BPA), phthalates, polychlorinated biphenyls (PCBs) and polybrominated diphenyl ethers (PBDEs) during these critical windows can reprogram endocrine and neural circuits, resulting in persistent behavioral alterations. This review synthesizes mechanistic evidence from animal models and epidemiological studies linking developmental EDC/POP exposure to attention deficits, impulsivity, anxiety and altered reward sensitivity-phenotypes defined here as addiction vulnerability (addiction-relevant endophenotypes) rather than clinically diagnosed substance-use disorder (SUD). We propose a two-hit, adverse outcome pathway (AOP)-informed model in which prenatal EDC/POP exposure induces endocrine-related perturbations that prime reward and stress circuitry. Subsequent exposure to psychoactive drugs and/or chronic stress then acts on these sensitized systems to increase the probability of maladaptive reinforcement learning and impaired behavioral control. Mechanistically, early-life exposures disrupt thyroid and sex-steroid signaling, dysregulate the hypothalamic-pituitary-adrenal axis, and alter dopaminergic, serotonergic, and glutamatergic neurotransmission with additional modulation by epigenetic reprogramming, oxidative stress, and neuroinflammation. Human cohort studies consistently associate prenatal BPA and phthalate exposures with adverse neurobehavioral and externalizing symptoms in children, supporting this framework while underscoring the limited availability of longitudinal data linking early exposure to SUD outcomes. Integrating these findings within an AOP perspective highlights the importance of developmental timing, sex, dose, genetic background, and co-exposures, and supports risk-assessment strategies that account for sequential environmental and drug exposures.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 3","pages":"471-490"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13149046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147761056","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":"Hypoxia Preserves Chromatin Integrity and Delays Cellular Senescence through Epigenetic Regulation.","authors":"Chansang Park, Hyunsung Park","doi":"10.4062/biomolther.2026.014","DOIUrl":"10.4062/biomolther.2026.014","url":null,"abstract":"<p><p>Hypoxia is a physiologically relevant microenvironment in both normal and diseased tissues and has emerged as a potent modulator of cellular senescence and organismal longevity. This review synthesizes evidence that hypoxia delays senescence across diverse experimental systems and species, and highlights mechanisms by which hypoxia rewires chromatin states during senescence-associated transitions. We focus on oxygen- and α-ketoglutarate-dependent epigenetic regulators, particularly histone lysine demethylases, whose catalytic activities are limited under hypoxia. Consequently, histone methylation increases and higher-order chromatin organization is stabilized. Using oncogene-induced senescence as an experimentally tractable framework, we discuss recent findings showing that hypoxia suppresses senescence-associated histone clipping, preserves nuclear lamina integrity, and restrains large-scale heterochromatin reorganization while leaving canonical cell-cycle arrest largely intact. We further consider emerging links among DNA damage, epigenetic instability, and aging phenotypes, and propose that senescence can be viewed as a breakdown of coordinated epigenetic homeostasis. By integrating these concepts, we position hypoxia and hypoxia-mimetic interventions as promising strategies to modulate aging-associated cellular states and to explore therapeutic opportunities in age-related pathologies.</p>","PeriodicalId":8949,"journal":{"name":"Biomolecules & Therapeutics","volume":"34 2","pages":"249-263"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12961988/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147301978","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}