Sehwan Kim, Junwoo Park, Hyemi Eo, Gi Beom Lee, Se Min Park, Minsang Shin, Seung Eun Lee, Youngpyo Nam, Sang Ryong Kim
{"title":"Intracerebellar upregulation of Rheb(S16H) ameliorates motor dysfunction in mice with SCA2.","authors":"Sehwan Kim, Junwoo Park, Hyemi Eo, Gi Beom Lee, Se Min Park, Minsang Shin, Seung Eun Lee, Youngpyo Nam, Sang Ryong Kim","doi":"10.1038/s41401-025-01504-y","DOIUrl":"10.1038/s41401-025-01504-y","url":null,"abstract":"<p><p>Cerebellar ataxia (CA) is characterized by impaired balance and coordination due to the loss of cerebellar neurons caused by various factors, and effective treatments are currently lacking. Recently, we observed reduced expression of signaling molecules in the mammalian target of rapamycin complex 1 (mTORC1) pathway in the cerebellum of mice with spinocerebellar ataxia type 2 (SCA2) compared with wild-type mice. To investigate the effects of mTORC1 upregulation on motor dysfunction in mice with SCA2, we administered an intracerebellar injection of adeno-associated virus serotype 1 carrying a constitutively active form of Ras homolog enriched in brain [Rheb(S16H)], which is an upstream activator of mTORC1. This treatment led to increased Rheb(S16H) expression in calbindin-D28K-positive Purkinje cells and increased levels of neurotrophic factors. Additionally, Rheb(S16H) upregulation reduced abnormal behaviors and protected Purkinje cells in mice with SCA2. Our findings suggest that upregulating Rheb(S16H) in the cerebellum may be a promising therapeutic strategy for hereditary CA.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1852-1863"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205046/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143539961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Lin Ai, Yi Han, Ting Ge, Sha Sha, Xiao-Jing Zhai, Ran Ji, Yu Zhou, Dan-Dan Chen, An Xie, Wen-Xin Zhang, Zhou Wu, Mo-Ruo Zhang, Jun-Xia Yang, An-Kang Hu, Jun-Li Cao, Ling-Zhen Song, Hong-Xing Zhang
{"title":"Dorsal raphe GABA-ergic neurons regulate the susceptibility to social transfer of pain in mice.","authors":"Lin Ai, Yi Han, Ting Ge, Sha Sha, Xiao-Jing Zhai, Ran Ji, Yu Zhou, Dan-Dan Chen, An Xie, Wen-Xin Zhang, Zhou Wu, Mo-Ruo Zhang, Jun-Xia Yang, An-Kang Hu, Jun-Li Cao, Ling-Zhen Song, Hong-Xing Zhang","doi":"10.1038/s41401-025-01494-x","DOIUrl":"10.1038/s41401-025-01494-x","url":null,"abstract":"<p><p>Some individuals are more susceptible to developing or suffering from pain states than others. However, the brain mechanisms underlying the susceptibility to pain responses are unknown. In this study, we defined pain susceptibility by recapitulating inter-individual differences in pain responses in mice exposed to a paradigm of socially transferred allodynia (STA), and with a combination of chemogenetic, molecular, pharmacological and electrophysiological approaches, we identified GABA-ergic neurons in the dorsal raphe nucleus (DRN) as a cellular target for the development and maintenance of STA susceptibility. We showed that DRN GABA-ergic neurons were selectively activated in STA-susceptible mice when compared with the unsusceptible (resilient) or control mice. Chemogenetic activation of DRN GABA-ergic neurons promoted STA susceptibility; whereas inhibiting these neurons prevented the development of STA susceptibility and reversed established STA. In in vitro slice electrophysiological analysis, we demonstrated that melanocortin 4 receptor (MC4R) enriched in DRN GABA-ergic neurons was a molecular target for regulating pain susceptibility, possibly by affecting DRN GABA-ergic neuronal activity. These results establish the DRN GABA-ergic neurons as an essential target for controlling pain susceptibility, thus providing important information for developing conceptually innovative and more accurate analgesic strategies.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1892-1904"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205041/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Kun Wang, Hui-Qiang Wang, Ge Yang, Shuo Wu, Hai-Yan Yan, Meng-Yuan Wu, Yu-Huan Li, Jian-Dong Jiang
{"title":"Carrimycin exhibited broad spectrum inhibitory activities against coronaviruses replication through down-regulating host factor TMEM41B.","authors":"Kun Wang, Hui-Qiang Wang, Ge Yang, Shuo Wu, Hai-Yan Yan, Meng-Yuan Wu, Yu-Huan Li, Jian-Dong Jiang","doi":"10.1038/s41401-025-01577-9","DOIUrl":"10.1038/s41401-025-01577-9","url":null,"abstract":"<p><p>We previously reported that carrimycin could inhibit pan-coronavirus including HCoV-229E, HCoV-OC43 and SARS-CoV-2. We found that carrimycin targeted the post-entry replicative events in coronavirus infection. Carrimycin could impede the viral protein translation switch from ORF1a to ORF1b by targeting programmed -1 ribosomal frameshifting (-1PRF). Carrimycin could also inhibit the newly synthesized (nascent) viral RNA. In this study we investigated whether carrimycin also inhibited the newly emerged SARS-CoV-2 variants. We showed that carrimycin (1.25-10 µM) dose-dependently inhibited both viral RNA and protein levels in Vero E6 cells. We further demonstrated that carrimycin disrupted the formation of SARS-CoV-2 double membrane vesicles (DMVs), and identified the host transmembrane protein B (TMEM41B) as the key factor involved in this process. Overexpression of TMEM41B increased viral protein levels and mRNA levels, whereas TMEM41B knockdown reduced viral replication including HCoV-229E, HCoV-OC43 and SARS-CoV-2. Moreover, overexpression of TMEM41B partially reversed the inhibitory effect of carrimycin, suggesting that carrimycin indeed exerted antiviral effects through regulation of TMEM41B. We revealed that carrimycin directly bound to TMEM41B and induced its K48 ubiquitination degradation, thereby inhibiting viral replication. These results expand the understanding of carrimycin's antiviral mechanisms, particularly its antiviral activity, and enrich our knowledge about the role of host factors in regulating viral replication.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"2006-2015"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205063/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144075239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"YY1/HIF-1α/mROS positive-feedback loop exacerbates glomerular mesangial cell proliferation in mouse early diabetic kidney disease.","authors":"Ting-Ting Yang, Yu-Ting Shao, Qian Cheng, Yu-Tian He, Zhen Qiu, Dan-Dan Pan, Huan-Ming Zhang, Zhen-Zhou Jiang, Meng Yan, Chang-Jiang Ying, Bao-Jing Li, Jun-Jie Liu, Si-Tong Qian, Tao Wang, Xiao-Xing Yin, Qian Lu","doi":"10.1038/s41401-025-01498-7","DOIUrl":"10.1038/s41401-025-01498-7","url":null,"abstract":"<p><p>Mesangial cells (MCs) are the most active intrinsic cells in the glomerulus. MCs excessively proliferate at the early stage of diabetic kidney disease (DKD), eventually causing glomerular sclerosis and even renal failure; inhibiting glomerular MC proliferation in early DKD is a promising prevention and treatment strategy for early DKD. Our previous study shows that Yin Yang 1 (YY1), a zinc finger protein, is a novel regulator of DKD-induced renal fibrosis. In this study we investigated the role of YY1 in glomerular MC proliferation in DKD in vivo and in vitro. We first showed that YY1 expression levels were significantly increased in the glomerular MCs of DKD patients and db/db mice and in high glucose (HG)-treated SV40-MES13 cells. By using YY1 expression/knockdown plasmids, we confirmed that YY1 contributed to glomerular MC proliferation in vitro. We demonstrated that YY1 upregulated hypoxia-inducible factor-1 alpha (HIF-1α) expression and activity in HG-treated SV40-MES13 cells, leading to overproduction of mROS. Moreover, mROS contributed to positive feedback regulation of YY1/HIF-1α signaling, and the YY1/HIF-1α/mROS positive feedback loop exacerbated glomerular MC proliferation in HG-treated SV40-MES13 cells. In addition, renal-specific YY1 overexpression promoted glomerular MC proliferation in normal mice, whereas renal-specific YY1 knockdown mitigated MC proliferation in early diabetic mice by inactivating HIF-1α/ROS signaling. In conclusion, the YY1/HIF-1α/mROS positive feedback loop might be an attractive therapeutic target for overcoming glomerulosclerosis in early DKD.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1974-1989"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205067/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143555592","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Costunolide normalizes neuroinflammation and improves neurogenesis deficits in a mouse model of depression through inhibiting microglial Akt/mTOR/NF-κB pathway.","authors":"Shao-Qi Zhang, Qiao Deng, Cheng Tian, Huan-Huan Zhao, Li-Ying Yang, Xin-Wei Cheng, Guo-Ping Wang, Dong Liu","doi":"10.1038/s41401-025-01506-w","DOIUrl":"10.1038/s41401-025-01506-w","url":null,"abstract":"<p><p>Neuroinflammation is crucial for the pathogenesis of major depression. Preclinical studies have shown the potential of anti-inflammatory agents, specifically costunolide (COS), correlate with antidepressant effects. In this study, we investigated the molecular mechanisms underlying the antidepressant actions of COS. Chronic restraint stress (CRS) was induced in male mice. The mice were treated with either intra-DG injection of COS (5 μM, 1 μL per side) or COS (20 mg/kg, i.p.) for 1 week. We showed that administration of COS through the both routes significantly ameliorated the depressive-like behavior in CRS-exposed mice. Furthermore, administration of COS significantly improved chronic stress-induced adult hippocampal neurogenesis deficits in the mice through attenuating microglia-derived neuroinflammation. We demonstrated that COS (5 μM) exerted anti-neuroinflammatory effects in LPS-treated BV2 cells via inhibiting microglial Akt/mTOR/NF-κB pathway; inactivation of mTOR/NF-κB/IL-1β pathway was required for the pro-neurogenic action of COS in CRS-exposed mice. Our results reveal the antidepressant mechanism of COS that is normalizing neuroinflammation to improve neurogenesis deficits, supporting anti-inflammatory agents as a potential therapeutic strategy for depression.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1864-1876"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205059/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514327","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Wen-Sheng Yang, Qing Liu, Yang Li, Guan-Yi Li, Shi Lin, Jie Li, Lin-Yu Li, Yuan Li, Xi-Lin Ge, Xiao-Zhen Wang, Wei Wu, Jun Yan, Guang-Fei Wang, Qing-Tong Zhou, Qiang Liu, Ming-Wei Wang, Zhi-Ping Li
{"title":"Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease.","authors":"Wen-Sheng Yang, Qing Liu, Yang Li, Guan-Yi Li, Shi Lin, Jie Li, Lin-Yu Li, Yuan Li, Xi-Lin Ge, Xiao-Zhen Wang, Wei Wu, Jun Yan, Guang-Fei Wang, Qing-Tong Zhou, Qiang Liu, Ming-Wei Wang, Zhi-Ping Li","doi":"10.1038/s41401-025-01525-7","DOIUrl":"10.1038/s41401-025-01525-7","url":null,"abstract":"<p><p>Current treatments of inflammatory bowel disease (IBD) largely depend on anti-inflammatory and immunosuppressive strategies with unacceptable efficacy and adverse events. Resolution or repair agents to treat IBD are not available but potential targets like formyl peptide receptor 2 (FPR2/ALX) may fill the gap. In this study we evaluated the therapeutic effects of two small molecule FPR2/ALX modulators (agonist Quin-C1 and antagonist Quin-C7) against IBD. We first analyzed the cryo-electron microscopy structure of the Quin-C1-FPR2 in complex with heterotrimeric G<sub>i</sub> to reveal the structural basis for ligand recognition and FPR2 activation. We then established dextran sulfate sodium (DSS)-induced colitis model in both normal and myeloid depletion mice. We showed that oral administration of Quin-C1 for 7 days ameliorated DSS-induced colitis evidenced by alleviated disease activity indexes, reduced colonic histopathological scores, and corrected cytokine disorders. Meanwhile, we found that oral administration of FPR2/ALX antagonist Quin-C7 exerted therapeutic actions similar to those of Quin-C1. In terms of symptomatic improvements, the ED<sub>50</sub> values of Quin-C1 and Quin-C7 were 1.3660 mg/kg and 2.2110 mg/kg, respectively. The underlying mechanisms involved ERK- or ERK/JNK-mediated myeloid cell regulation that limited the development of colitis and inflammation. This is the first demonstration of anti-colitis property caused by synthetic small molecule FPR2/ALX modulators, implying that FPR2/ALX modulation rather than agonism alone ameliorates IBD.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1958-1973"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205095/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603189","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Yong-Hao Li, Chu-Run Zheng, Yue Liu, Ke Wang, Fan-Fan Zhou, Xin Dong, Tao Yuan, Qiao-Jun He, Hong Zhu, Bo Yang
{"title":"The role of calcium signaling in organotropic metastasis of cancer.","authors":"Yong-Hao Li, Chu-Run Zheng, Yue Liu, Ke Wang, Fan-Fan Zhou, Xin Dong, Tao Yuan, Qiao-Jun He, Hong Zhu, Bo Yang","doi":"10.1038/s41401-025-01537-3","DOIUrl":"10.1038/s41401-025-01537-3","url":null,"abstract":"<p><p>Tumor metastasis is an important event in cancer progression, representing an enduring and irrevocable hallmark of cancers. The causes of tumor metastasis are complex and diverse. Arising evidence shows that the dysregulation of calcium signaling plays a crucial role in its initiation and progress. Calcium is an essential secondary messenger that regulates signaling pathways associated with tumor metastasis. The transient accumulation of calcium potentially promotes the advancement of tumor metastasis, while calcium-dependent proteins and calcium-related channels also significantly contribute to such malignant process. Thus, compounds specially targeting calcium channels, transporters or pumps may be therapeutic approaches prohibiting tumor metastasis. This review focuses on exploring the roles of calcium ions, calcium-dependent proteins and calcium-related channels in organotropic metastasis of cancer and its clinical applications in the treatment of metastatic cancers.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1801-1812"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205096/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143708032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Su-Lan Yu, Mei-Ling Wu, Philip Hei Li, Ya-Cun Chen, Jing Xie, Xiao-Yu Xu, Dan-Bao Ma, Yun Feng, Jian-Gang Shen, Xiang Lin
{"title":"Calycosin synergizes with methotrexate in the treatment of Sjögren's disease by targeting BATF in T follicular helper cells.","authors":"Su-Lan Yu, Mei-Ling Wu, Philip Hei Li, Ya-Cun Chen, Jing Xie, Xiao-Yu Xu, Dan-Bao Ma, Yun Feng, Jian-Gang Shen, Xiang Lin","doi":"10.1038/s41401-025-01536-4","DOIUrl":"10.1038/s41401-025-01536-4","url":null,"abstract":"<p><p>T follicular helper (Tfh) cells are crucially involved in the pathogenesis of autoimmune disorders, including Sjögren's disease (SjD, also known as Sjögren's syndrome), by promoting effector B cell responses and autoantibodies production. However, targeting Tfh cells remains challenging. In this study, we identified that calycosin (Caly), a natural flavonoid, effectively suppressed pathogenic Tfh cell responses, although it did not affect the plasmacytic differentiation of B cells. Under Tfh polarization conditions, Caly rapidly bound to the master transcription factor, BATF, in both human and murine CD4<sup>+</sup> T cells and thus potently disrupted BATF-mediated Maf gene transcription. Methotrexate (MTX), a first-line medication in the treatment of autoimmune disorders, mainly suppresses B cell responses but fails to target Tfh cells. In a mouse model of experimental Sjögren's syndrome (ESS) that we previously established, MTX synergized with Caly in attenuating the disease pathology and autoantibodies in ESS mice with chronic inflammation, with signs of disease remission. This immunomodulatory function was also validated in peripheral blood mononuclear cells from patients with SjD. Thus, Caly may serve as a novel inhibitor of BATF in suppressing Tfh-cell-mediated humoral autoimmunity and elicit a synergistic effect in combination with B-cell-targeting strategies.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1990-2005"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205085/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143778644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"FNDC5/Irisin exacerbates APAP-induced acute liver injury through activating JNK/NF-κB and inflammatory response.","authors":"Qian-Hui Zhang, Lei-Ming Jin, Meng-Sha Lin, Min-Xiu Wang, Ya-Qian Cui, Jia-Xi Ye, Yong-Qiang Xiong, Wu Luo, Wei-Wei Zhu, Guang Liang","doi":"10.1038/s41401-025-01509-7","DOIUrl":"10.1038/s41401-025-01509-7","url":null,"abstract":"<p><p>Acute liver injury (ALI) is associated with high mortality rates. Despite its severity, there are currently no effective interventions, underscoring the urgent need for research on the mechanisms driving ALI progression. Irisin, a hormone derived from its precursor FNDC5, has been shown to play a critical role in some chronic liver diseases. In this study we investigated the role of hepatic FNDC5/Irisin in a mouse model of AILI induced by acetaminophen (APAP, 400 mg/kg, i.p.). The mice were euthanized at 6, 12 and 24 h after APAP injection, then the blood and liver tissues were collected for analyses. By conducting transcriptome sequencing, we identified that both the expression and release of FNDC5/Irisin were significantly increased and highly correlated with AILI. We showed that knockout of Irisin significantly improved APAP-induced tissue damage and hepatocyte death in mouse liver. Conversely, preinjection of recombinant Irisin protein (1 mg·kg<sup>-1</sup>·d<sup>-</sup><sup>1</sup>, i.p., for 3 days) exacerbated the AILI in FNDC5 knockout mice. RNA-seq analysis revealed that knockout of FNDC5/Irisin reduced inflammatory responses and JNK/NF-κB activation in APAP-treated mouse liver, while exogenous Irisin administration aggravated JNK/NF-κB-mediated inflammation. In primary mouse hepatocytes treated with APAP (15 mM), application of Irisin (100 ng/mL) activated the integrin αV/JNK/NF-κB axis, driving inflammation and oxidative stress. In summary, this study highlights Irisin as a critical regulator in AILI progression. Circulating Irisin could be a novel biomarker for AILI diagnosis, and targeting FNDC5/Irisin could hold promise for the development of novel treatments for AILI.</p>","PeriodicalId":6942,"journal":{"name":"Acta Pharmacologica Sinica","volume":" ","pages":"1946-1957"},"PeriodicalIF":6.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12205071/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143522398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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