International immunopharmacology最新文献

{"title":"Paeoniflorin alleviates necroptosis in acute kidney injury induced by cisplatin and lansoprazole through targeting TNFAIP3.","authors":"Wei Zhu, Sai Zhu, Shan Jiang, Jiuyu Yin, Yonggui Wu, Xiaomei Luo","doi":"10.1016/j.intimp.2025.115340","DOIUrl":"10.1016/j.intimp.2025.115340","url":null,"abstract":"<p><strong>Background: </strong>Cisplatin (CIS), a widely administered chemotherapeutic agent, is associated with acute kidney injury (AKI). Lansoprazole (LPZ), commonly prescribed to mitigate chemotherapy-induced gastrointestinal complications, may further elevate AKI risk. Paeoniflorin (Pae), a bioactive compound derived from traditional Chinese medicine, demonstrates renal protective properties in AKI, yet its mechanism against CIS and LPZ induced AKI remains undefined.</p><p><strong>Methods: </strong>A composite AKI model was established in vivo and in vitro using CIS and LPZ. The protective effect of Pae on the injury of renal tissue or renal tubular cells in mice was observed, followed by Pae pretreatment. The target of Pae was found through network pharmacology, and the binding ability of the target was verified by CETSA experiment and molecular docking. Finally, the target gene was knocked out or over expressed to verified whether Pae regulates necroptosis through this target.</p><p><strong>Results: </strong>It was found that renal injury could be exacerbated by LPZ in the CIS induced AKI. Pae could alleviate CIS and LPZ induced AKI. The target gene of Pae was TNFAIP3, which played an important role in necroptosis. The TNFAIP3 could bind well to Pae in molecular docking and CETSA experiment. The necroptosis and inflammatory responses in AKI induced by CIS and LPZ could be also inhibited by Pae in vivo and in vitro. Overexpression of TNFAIP3 played the same cellular protective role as Pae preconditioning. In contrast, Pae could not continue to play a protective role after TNFAIP3 was knocked down.</p><p><strong>Conclusion: </strong>The traditional Chinese medicine Pae holds promise as a potential therapeutic agent for AKI, with TNFAIP3 representing an effective therapeutic target in this pathology.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115340"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804050","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"3C3 alleviates atopic dermatitis-like phenotypes through cyclophilin A and B-mediated inhibition of calcineurin-NFAT pathway.","authors":"Yejin Jo, Hayan Jeong, Su-Jin Lee, Jangho So, Seung-Heon Yoo, Soonnam Kim, Suyoung Go, Jee Yoon Shin, Yul Lee, Dong-Sik Shin, Seok-In Kim, Yoon-Sik Lee, Bong-Gun Ju","doi":"10.1016/j.intimp.2025.115335","DOIUrl":"10.1016/j.intimp.2025.115335","url":null,"abstract":"<p><p>Atopic dermatitis (AD) disrupts a patients' quality of life and is associated with other atopic disorders, such as food allergy, allergic rhinitis, and asthma. Although topical medications are widely used, they have undesirable side effects, suggesting the need for treatments with improved efficacy and safety. In this study, we identified 3C3 as a candidate compound for AD treatment using in vitro TNFα-treated HaCaT keratinocytes and a DNFB-induced AD mouse model. 3C3 treatment alleviated AD-like phenotypes and suppressed the gene activation of pro-inflammatory cytokine. We further found that 3C3 binds to cyclophilin A (CypA) and cyclophilin B (CypB), inhibiting the phosphatase activity of calcineurin. 3C3 treatment suppressed the nuclear translocalization and occupancy of NFAT2 and NFAT4 at gene promoters of IL-6, IL-13, IL-31, and IL-33 in PAR2 activated HaCaT keratinocytes. This resulted in suppression of PAR2 agonist-induced gene activation of IL-6, IL-13, IL-31, and IL-33. In addition, unlike glucocorticoids, 3C3 did not induce skin atrophy through upregulation of REDD1 and reduction of mTOR signaling. Our study suggests that 3C3 may help alleviate skin inflammatory diseases including AD, through a mechanism similar to that of cyclosporine A, whose use is limited due to side effects such as nephrotoxicity.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115335"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metformin mitigates inflammation and apoptosis in salivary gland epithelial cells via an AMPK-dependent mechanism in chronic obstructive sialadenitis.","authors":"Lianhao Wang, Boyuan Peng, Shijiao Pan, Jialing Kang, Bo Li, Yong Cheng","doi":"10.1016/j.intimp.2025.115345","DOIUrl":"10.1016/j.intimp.2025.115345","url":null,"abstract":"<p><p>Chronic obstructive sialadenitis (COS) frequently results from apoptosis and inflammation in salivary gland epithelial cells, leading to salivary secretion dysfunction. Our previous research suggested that metformin (MET) might have a protective effect on salivary gland epithelial cells, but the underlying mechanism remains unclear. This study investigated the potential impact of MET on COS using human salivary gland tissues, an in vitro inflammatory cell model, and a Wharton's ductal ligation model. Western blot, immunohistochemistry, and immunofluorescence were employed to assess protein expression and phosphorylation. Terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining and Annexin V-FITC/PI double staining were used to assess cell apoptosis. Signaling pathways potentially affected by MET were assessed by RNA sequencing. The results showed that MET could attenuate LPS-induced cell apoptosis and inflammation in a dose-dependent manner, including increasing the Bcl-2/Bax ratio, inhibiting caspase-3 activation, reducing NF-κB p65 phosphorylation, and decreasing IL-1β and TNF-α levels. Moreover, we observed reduced AMPK phosphorylation in COS patient tissues, and AMPK inhibition reversed the regulation of MET's effect on NF-κB p65 phosphorylation and caspase-3. In the Wharton's ductal ligation model, MET mitigated ligation-induced cell apoptosis and inflammatory responses. These findings suggest that MET activates AMPK to attenuate apoptosis and inflammatory responses in salivary gland epithelial cells, offering a new therapeutic strategy for COS.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115345"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144821390","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted delivery of Bak BH3 peptide to renal myofibroblast for renal fibrosis treatment by activating the mitochondrial-dependent apoptosis pathway.","authors":"Xiaohua Wang, Liming Xu, Lingxin Kong, Xiaohui Liu, Xiaowen Qiu, Jiaru Zhang, Baitong Chang, Mengxin Yao, Yunting Xu, Xiaohuan Yuan, Haifeng Liu","doi":"10.1016/j.intimp.2025.115324","DOIUrl":"10.1016/j.intimp.2025.115324","url":null,"abstract":"<p><strong>Background: </strong>Renal fibrosis is positively associated with the increased number of renal myofibroblasts with over-expressed platelet-derived growth factor β receptor (PDGFβR). Reducing the number of renal myofibroblasts by inducing cell apoptosis is a novel strategy for treating renal fibrosis. The functional domain BH3 from protein Bak (BH3 peptide) exerts pro-apoptotic activity and the affibody Z_PDGFβR shows a superior high affinity for PDGFβR. This study aimed to evaluate renal fibrosis treatment by targeting delivery of BH3 to fibrotic kidney using Z_PDGFβR as a carrier.</p><p><strong>Methods: </strong>The targeting potential of Z-BH3 (BH3 genetically fused to Z_PDGFβR) on the TGF-β1-activated NIH3T3 cell model and UUO mice model of renal fibrosis were evaluated by fluorescence-tracer imaging. Anti-renal fibrosis effect of Z-BH3 on kidney fibrosis in vitro and in vivo was evaluated by TUNEL, ROS, immunofluorescence, immunohistochemical and pathological staining and western blot.</p><p><strong>Results: </strong>Z-BH3 highly targeted activated NIH3T3 cells and fibrotic kidney from UUO mice. Z-BH3 significantly induced cell apoptosis, reduced the fibrosis-related protein levels in activated NIH3T3 cells. Z-BH3 markedly promoted cell apoptosis, attenuated the pathological changes, and mitigated fibrosis responses in UUO mice. Z-BH3 remarkably reduced the mitochondrial membrane potential (MMP), increased the levels of pro-apoptotic Bax, cleaved caspase-3 and PARP as well as ROS generation, and inhibited anti-apoptotic Bcl-2 expressions in vitro and in vivo.</p><p><strong>Conclusion: </strong>Z-BH3 attenuated renal fibrosis in vitro and in vivo by targeting induction of cell apoptosis in renal myofibroblasts via the mitochondrial-dependent pathway. This study provides a novel avenue for renal fibrosis therapy.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115324"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144804051","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"5-aminolaevulinic acid combined with sodium ferrous citrate ameliorated collagen-induced arthritis via anti-inflammatory effects and fibroblast-like synoviocytes-driven B cell immunomodulation.","authors":"Zhaolun Ding, Kuai Ma, Atsuko Kamiya, Hidenori Ito, Kiwamu Takahashi, Motowo Nakajima, Chunsheng Wang, Masayuki Fujino, Xiao-Kang Li","doi":"10.1016/j.intimp.2025.115320","DOIUrl":"10.1016/j.intimp.2025.115320","url":null,"abstract":"<p><strong>Purpose: </strong>This study evaluated the therapeutic potential of 5-aminolevulinic acid combined with sodium ferrous citrate (5-ALA/SFC) for rheumatoid arthritis (RA), focusing on its dual anti-inflammatory and immunomodulatory properties.</p><p><strong>Methods: </strong>Collagen-induced arthritis (CIA) murine models were administered either low (100/157 mg/kg) or high (500/157 mg/kg) doses of 5-ALA/SFC. Disease progression was evaluated using clinical scoring, a histopathological analysis, and micro-computed tomography to assess bone morphology. Synovial inflammation and oxidative stress markers, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, inducible nitric oxide synthase (iNOS), heme oxygenase-1 (HO-1), and indoleamine 2,3-dioxygenase (IDO), were quantified in fibroblast-like synoviocytes (FLSs) using flow cytometry and quantitative reverse transcription polymerase chain reaction. B cell subpopulations, specifically plasmablasts and regulatory B cells (Bregs) in the draining lymph nodes (dLNs), were analyzed by flow cytometry. Human MH7A synovial cells were used to corroborate the FLS-mediated immunoregulatory effects.</p><p><strong>Results: </strong>5-ALA/SFC demonstrated significant dose-dependent amelioration of joint swelling, synovial hyperplasia, cartilage, and bone degradation in CIA mice. This treatment significantly attenuated the expression of pro-inflammatory mediators (TNF-α, IL-1β, and iNOS) in FLSs while upregulating the expression of HO-1, IDO, and TNF-stimulated gene-6 (TSG-6). In the dLNs, 5-ALA/SFC reduced the proportion of plasmablasts and increased the percentage of Bregs. In vitro experiments using MH7A cells confirmed that 5-ALA/SFC downregulates B cell-activating factor (BAFF) and vascular cell adhesion molecule-1 (VCAM-1), both of which are critical for B cell maturation, and enhances HO-1 and TSG-6 expression under pro-inflammatory cytokine stimulation.</p><p><strong>Conclusion: </strong>5-ALA/SFC exerted its therapeutic effects in RA by suppressing synovial inflammation via HO-1/IDO-mediated antioxidant pathways and restoring B cell homeostasis by modulating FLS-derived signals, including BAFF and VCAM-1 in mice. Potential translational limitations include inherent differences between murine CIA models and human RA pathophysiology, as well as the use of immortalized human synovial cell lines instead of primary patient-derived FLSs. These findings underscore the potential of 5-ALA/SFC as a multitarget therapeutic strategy, offering promising prospects for the development of novel RA treatments though clinical translation requires further investigation of long-term safety, optimal dosing, and side effects in humans.</p>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"164 ","pages":"115320"},"PeriodicalIF":4.7,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144816532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sigma-1 receptor activation ameliorates age-related postoperative cognitive dysfunction by attenuating endoplasmic reticulum stress and neuroinflammation","authors":"Yabo Hao ,&nbsp;Rui Hao ,&nbsp;Kai Lu ,&nbsp;Yun He ,&nbsp;Zhao Xu","doi":"10.1016/j.intimp.2025.115677","DOIUrl":"10.1016/j.intimp.2025.115677","url":null,"abstract":"<div><div>Postoperative Cognitive Dysfunction (POCD), a key phenotype within the broader spectrum of Postoperative Neurocognitive Disorders (PND), represents a significant neurological complication, predominantly affecting elderly individuals and resulting in cognitive impairment and diminished quality of life. The Sigma-1 receptor (Sigma-1R), a critical modulator of cellular stress endowed with neuroprotective properties, has emerged as a potential therapeutic target. This investigation aimed to elucidate the role of Sigma-1R in age-related susceptibility to POCD and to assess the therapeutic efficacy of the Sigma-1R agonist, PRE-084. Employing an exploratory laparotomy mouse model of POCD, we evaluated age-dependent variations in hippocampal Sigma-1R expression, its specific cellular localization, and the effects of PRE-084 administration on cognitive performance and associated molecular pathways in aged mice. Our findings revealed significantly lower basal hippocampal Sigma-1R levels in aged mice compared to their adult counterparts. Subsequent to surgical intervention, adult mice demonstrated a robust upregulation of Sigma-1R, which correlated with preserved cognitive function. In contrast, aged mice exhibited a blunted Sigma-1R response (a non-significant trend towards an increase), correlating with more pronounced cognitive deficits. Immunohistochemical analysis confirmed predominant Sigma-1R expression within hippocampal neurons. Post-surgical administration of PRE-084 to aged mice resulted in a substantial amelioration of cognitive function, as assessed by the Morris water maze. These salutary effects were associated with an attenuation of endoplasmic reticulum (ER) stress, evidenced by reduced levels of BIP and p-eIF2α, mitigation of neuroinflammation, indicated by decreased microglial and astrocytic activation, inhibition of NF-κB activation, and promotion of CREB phosphorylation. In conclusion, this study underscores the pivotal role of a differential Sigma-1R response to surgical stress in the pathogenesis of age-related POCD. PRE-084 demonstrates promise as a therapeutic agent, exerting neuroprotection by alleviating neuronal ER stress, which in turn curtails secondary neuroinflammation and recalibrates critical NF-κB and CREB signaling pathways.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"167 ","pages":"Article 115677"},"PeriodicalIF":4.7,"publicationDate":"2025-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145270473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Bioactive peptides PIISVYWK and FSVVPSPK improve glucose homeostasis by targeting DPP-IV and glucose transport in type 2 diabetic mice\" [Int. Immunopharmacol. 158 (2025) 114844].","authors":"Indyaswan T Suryaningtyas, Won-Kyo Jung, Sei-Jung Lee, Jae-Young Je","doi":"10.1016/j.intimp.2025.115326","DOIUrl":"10.1016/j.intimp.2025.115326","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115326"},"PeriodicalIF":4.7,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812035","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Tumor-induced thymic involution via inhibition of IL-7Rα and its JAK-STAT signaling pathway: Protection by black tea\" [Int. Immunopharmacol. 6(3) (2006) 433-444].","authors":"Debaprasad Mandal, Lakshmishri Lahiry, Arindam Bhattacharyya, Sankar Bhattacharyya, Gaurisankar Sa, Tanya Das","doi":"10.1016/j.intimp.2025.115409","DOIUrl":"10.1016/j.intimp.2025.115409","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115409"},"PeriodicalIF":4.7,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144953207","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"2,3,5,6-Tetrafluoro-4-Methoxy-Benzamide alleviates idiopathic pulmonary fibrosis through activation of LGALS3-mediated AGE-RAGE signaling pathway","authors":"Yikun Chen ,&nbsp;Qing Liu ,&nbsp;Ran Fu ,&nbsp;Yucheng Liu ,&nbsp;Jiayi Shen ,&nbsp;Yi Wang","doi":"10.1016/j.intimp.2025.115635","DOIUrl":"10.1016/j.intimp.2025.115635","url":null,"abstract":"<div><div>Idiopathic pulmonary fibrosis (IPF), a progressive lung disease with limited therapeutic options, urgently requires novel treatment strategies. This study investigates the mechanism of 2,3,5,6-Tetrafluoro-4-Methoxy-Benzamide (TFMB) in alleviating IPF through LGALS3-mediated AGE-RAGE pathway. Demographic characteristics of IPF patients during 2020–2024 were analyzed. IPF mouse and cell models were induced by bleomycin (BLM) to evaluate the anti-fibrotic effects of TFMB, with validation by LGALS3/RAGE overexpression. Hematoxylin-eosin, Masson's trichrome and Sirius red staining were used to assess inflammatory infiltration and collagen deposition in lung tissues. Western blot, RT-qPCR, biochemical analysis, immunohistochemistry and ELISA were performed for molecular profiling. CCK-8 was employed for cell viability testing. Bioinformatics integration with KEGG/GO analyses were conducted to explore the potential regulatory mechanisms of TFMB. Immunoprecipitation (IP) was utilized to examine the binding between LGALS3 and AGE. Clinical data analysis revealed a progressive decline in the age of IPF patients. TFMB significantly inhibited inflammation infiltration, collagen deposition, and upregulated hydroxyproline content, fibroblast activation-related markers and LGALS3 expression in BLM-challenged mice. In vitro, TFMB suppressed BLM-induced upregulation of CTGF and CX3CL1 mRNA expression, fibroblast activation-related markers, and LGALS3 levels. LGALS3 overexpression abrogated TFMB's therapeutic effect on IPF. KEGG/GO analyses suggested involvement of AGE-RAGE pathway activation in IPF. IP found that LGALS3 bound to AGE, inhibiting AGE-RAGE pathway activation. RAGE overexpression rescued the diminished anti-fibrotic efficacy of TFMB under LGALS3 overexpression. TFMB alleviates IPF by inhibiting LGALS3, thereby suppressing AGE-RAGE signaling pathway activation. TFMB has the potential to be a novel therapeutic drug for IPF.</div></div>","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":"167 ","pages":"Article 115635"},"PeriodicalIF":4.7,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145270472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to \"Artesunate ameliorates ligature-induced periodontitis by attenuating NLRP3 inflammasome-mediated osteoclastogenesis and enhancing osteogenic differentiation\" [Int. Immunopharmacol. 123 (2023) 110749].","authors":"Zhanqi Wang, Xuan Feng, Guorui Zhang, Haiyun Li, Feng Zhou, Yaxin Xie, Tianjiao Li, Chengzhi Zhao, Wenxin Luo, Yi Xiong, Yingying Wu","doi":"10.1016/j.intimp.2025.115454","DOIUrl":"10.1016/j.intimp.2025.115454","url":null,"abstract":"","PeriodicalId":13859,"journal":{"name":"International immunopharmacology","volume":" ","pages":"115454"},"PeriodicalIF":4.7,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000544","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}