Inflammopharmacology最新文献

{"title":"Iota-carrageenan oligosaccharide ameliorates DSS-induced colitis in mice by mediating gut microbiota dysbiosis and modulating SCFAs-PI3K-AKT pathway.","authors":"Meixian Xiang, Songtao Wu, Minxin Liu, Bin Zhang, Xiankun Xia, Wenjing Tan, Shijian Xiang","doi":"10.1007/s10787-025-01718-w","DOIUrl":"https://doi.org/10.1007/s10787-025-01718-w","url":null,"abstract":"<p><p>Iota-carrageenan oligosaccharides (iCOs), derived from marine red algae, are traditionally used as antithrombotic and anti-inflammatory agents in folk medicinal practice. Despite the prevailing emphasis on these aspects in their applications, the potential of iCOs as a prebiotic agent for gut health and its subsequent impact on intestinal disorders such as colitis remains largely unexplored. A DSS-induced colitis model was employed in C57BL/6 male mice to analyze the gut microbiota via 16S rRNA sequencing. Fecal microbiota transplantation (FMT) was used to assess the therapeutic effects of iCOs on colitis. RNA sequencing (RNA-Seq) identified pathways and genes affected by iCOs. ELISA measured inflammatory cytokines, while western blot and RT-qPCR evaluated protein and gene expressions, respectively. The iCOs increased beneficial bacteria, such as Lactobacillus, Bifidobacterium, and Akkermansia. They enhanced short-chain fatty acid production and upregulated GPR41, GPR43, and GPR109A mRNA, influencing cytokine secretion. The iCOs reduced mRNA of SPHK1, BDKRB1, LCN2, and so on, potentially through PI3K-Akt pathway inhibition, and promoted tight junction protein expression. Our findings highlight the novel therapeutic potential of iCOs in colitis, indicating a multifaceted approach to treatment that includes gut microbiota modulation, intestinal barrier restoration, and the suppression of inflammatory responses.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":""},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752506","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":"NLRP3 inflammasomes pathway: a key target for Metformin.","authors":"Yasamin Hosseini, Amirhossein Niknejad, Ayeh Sabbagh Kashani, Mahsa Gholami, Mahtab Roustaie, Mohammad Mohammadi, Saeideh Momtaz, Stephen L Atkin, Tannaz Jamialahmadi, Amir Hossein Abdolghaffari, Amirhossein Sahebkar","doi":"10.1007/s10787-025-01702-4","DOIUrl":"10.1007/s10787-025-01702-4","url":null,"abstract":"<p><p>Nucleotide-binding oligomerization domain, Leucine rich Repeat and Pyrin domain containing 3 (NLRP3) is a signaling pathway that is involved in inflammatory cascades, cell survival and the immune response. NLRP3 is activated by cellular damage, oxidative stress, and other factors that stimulate the immune system. Stimulation of NLRP3 induces inflammatory reactions and the production of inflammatory cytokines. These inflammatory mediators are implicated in several diseases. Metformin (MET) is an anti-hyperglycemia agent that is extensively used in clinical practice worldwide due to its high efficiency, safety profile, and affordable price. MET is the only member of biguanide class that is used in clinical practice and a potent AMP-activated protein kinase (AMPK) agonist with proven anti-inflammatory characteristics. Due to its anti-inflammatory properties, MET is considered to be effective against diseases that have an inflammatory background, and the NLRP3 pathway is involved in the pathophysiology of these disorders. In this review, we have evaluated the evidence if MET can affect this pathway and its utility for future therapeutic approaches.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1729-1760"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556781","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":"Emerging treatments for dermatologic diseases in infants, children, and adolescents: a systematic review of clinical trials on biologics and small molecule inhibitors.","authors":"Alireza Jafarzadeh, Elham Behrangi, Mina Khosravi, Saba Falakeh, Jasmine Khalilnejad Amiri, Azadeh Goodarzi","doi":"10.1007/s10787-025-01675-4","DOIUrl":"10.1007/s10787-025-01675-4","url":null,"abstract":"<p><strong>Background: </strong>Recent advancements in the treatment of paediatric dermatological conditions have emerged with the introduction of biologics and small molecule inhibitors (SMIs). These therapies target specific inflammatory pathways, which may enhance treatment outcomes for diseases like atopic dermatitis, psoriasis, and alopecia areata.</p><p><strong>Objectives: </strong>This systematic review seeks to assess the effectiveness and safety of biologics and SMIs for dermatologic conditions in children and adolescents, with an emphasis on randomised clinical trials.</p><p><strong>Methods: </strong>We performed an extensive literature search across PubMed, Scopus, and Web of Science, following PRISMA guidelines. Studies included in the review were those that analysed systemic treatments using biologics and SMIs in subjects under 18 years of age. We extracted data on participant demographics, treatment regimens, effectiveness outcomes, adverse effects, and follow-up details. The risk of bias in the studies was determined using the Cochrane Risk of Bias Tool (RoB2).</p><p><strong>Results: </strong>From an initial pool of 1,454 studies, 49 articles fitting the inclusion criteria were identified, encompassing 6372 cases. The review found that biologics such as Dupilumab, along with investigational JAK inhibitors like Abrocitinib and Upadacitinib, exhibited considerable efficacy in treating various conditions, particularly atopic dermatitis and psoriasis. Dupilumab specifically demonstrated significant improvements in both disease severity and quality of life. While most reported adverse events were mild to moderate, some serious adverse events were noted with certain treatments.</p><p><strong>Conclusions: </strong>Biologics and SMIs show great promise as therapeutic options in paediatric dermatology, offering better efficacy compared to traditional treatments. Despite these encouraging findings, additional research is needed to verify their long-term safety, especially in relation to growth and development in younger patients. Future investigations should aim to include a broader range of patient demographics and dermatological conditions beyond those currently studied.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1617-1672"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143556777","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":"Insulin resistance in Alzheimer's disease: signalling mechanisms and therapeutics strategies.","authors":"Mini Dahiya, Monu Yadav, Chetan Goyal, Anil Kumar","doi":"10.1007/s10787-025-01704-2","DOIUrl":"10.1007/s10787-025-01704-2","url":null,"abstract":"<p><strong>Background: </strong>Alzheimer's disease (AD), one of the most common neurodegenerative disorders, is characterised by hallmark abnormalities such as amyloid-β plaques and neurofibrillary tangles (NFTs). Emerging evidence suggests that faulty insulin signalling contributes to these pathological features, impairing critical cellular and metabolic processes.</p><p><strong>Objective: </strong>This review aims to elucidate the role of insulin signalling in the central nervous system (CNS) under normal and pathological conditions and to explore therapeutic approaches targeting insulin pathways in AD and other neurodegenerative diseases.</p><p><strong>Methods: </strong>We reviewed studies highlighting the involvement of insulin-signalling pathways in neuronal health, with a particular focus on the key components-IRS, PI3K, Akt, and GSK-3β-predominantly expressed in cortical and hippocampal regions.</p><p><strong>Results: </strong>Insulin, an essential growth factor, regulates numerous cellular functions, including glucose metabolism, mitochondrial activity, oxidative stress response, autophagy, synaptic plasticity, and cognitive processes. Altered phosphorylation of signalling molecules in insulin pathways contributes to oxidative stress, inflammation, and the formation of AD hallmarks. Indirect modulators such as NF-κB and caspases further exacerbate neuronal damage, linking impaired insulin signalling to neurodegeneration.</p><p><strong>Conclusion: </strong>Insulin signalling plays a crucial role in maintaining neuronal health and mitigating neurodegenerative processes. Targeting insulin pathways and associated molecules offers promising therapeutic avenues for AD and other neurodegenerative disorders.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1817-1831"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143597125","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":"Kirenol ameliorates endotoxin-induced acute lung injury by inhibiting the ERK and JNK phosphorylation-mediated NFκB pathway in mice.","authors":"Frank Cheau-Feng Lin, Shih-Pin Chen, Sheng-Chien Lin, Ching-Chi Tseng, Stella Chin-Shaw Tsai, Yu-Hsiang Kuan","doi":"10.1007/s10787-025-01693-2","DOIUrl":"10.1007/s10787-025-01693-2","url":null,"abstract":"<p><p>Acute lung injury (ALI) is a pathological condition characterised by varying degrees of lung damage in patients. Kirenol exerts anti-inflammatory, immunosuppressive, and antioxidative effects. We investigated the protective effects of kirenol on lipopolysaccharide-induced ALI in mice. Pretreatment with kirenol significantly ameliorated lung oedema and neutrophil infiltration in ALI mice. Kirenol downregulated the chemokines (MIP-2) expression and the adhesion molecules (ICAM-1 and VCAM-1) secretion. Furthermore, kirenol inhibited the production of the proinflammatory mediators nitric oxide and prostaglandin (PG)E2 through the upstream factors iNOS and cyclooxygenase (COX)-2, respectively. Kirenol suppressed the IKK-IκB-NFκB pathway, which is involved in lipopolysaccharide-induced inflammation. Kirenol inhibited the lipopolysaccharide-induced phosphorylation of ERK and JNK, to a lesser extent, p38 MAPK and Akt. In conclusion, our findings suggest that kirenol exerts ameliorative effects against ALI by suppressing the production of chemokines, adhesion molecules, and proinflammatory mediators and inhibiting the IKK-IκB-NFκB pathway and its upstream factors, phosphorylated ERK and JNK.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2069-2081"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143541813","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":"Sodium hyaluronate and acupotomy bone decompression alleviates inflammatory responses in patients with knee osteoarthritis.","authors":"Jia Wu, Qiong Tang, Xiaofei Tan","doi":"10.1007/s10787-025-01667-4","DOIUrl":"10.1007/s10787-025-01667-4","url":null,"abstract":"<p><strong>Objective: </strong>Knee osteoarthritis (KOA), predominantly affecting middle-aged and elderly populations, induces localized joint pain and functional impairment. It was to evaluate the effectiveness of acupotomy bone decompression (ABD) combined with sodium hyaluronate (SH) intra-articular injection on inflammatory responses in treating KOA.</p><p><strong>Methods: </strong>Clinical data from 128 patients with KOA were retrospectively collected, categorized into SH group (n = 55) and ABD + SH group (n = 73). Pain was assessed using the visual analogue scale (VAS), knee joint function was evaluated, and knee joint balance and gait parameters were measured. The status of articular cartilage and bone marrow edema was evaluated using quantitative magnetic resonance imaging (MRI). Interleukin (IL)-6, IL-1β, tumor necrosis factor (TNF)-α, matrix metalloproteinase (MMP)-3, MMP-9, and hypersensitive C-reactive protein (hs-CRP) were detected.</p><p><strong>Results: </strong>ABD + SH group showed drastic reductions in VAS scores, decreased indices of different axial balances, and increased stride length and walking speed versus the SH group (P < 0.05). Quantitative MRI examination revealed that relative to the SH group, ABD + SH group exhibited increased thickness of articular cartilage and reduced area of bone marrow edema post-treatment (P < 0.05). Post-treatment levels of hs-CRP, IL-6, IL-1β, TNF-α, MMP-3, and MMP-9 were markedly lower in the ABD + SH group versus SH group (P < 0.05). Moreover, the clinical effective rate in the ABD + SH group was drastically superior to the SH group (95.9% vs. 78.2%, P < 0.05).</p><p><strong>Conclusion: </strong>Combining ABD with SH treatment for KOA effectively alleviates patient pain and inflammatory responses.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1997-2005"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143457699","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":"Targeting TGF-β/VEGF/NF-κB inflammatory pathway using the Polyphenols of Echinacea purpurea (L.) Moench to enhance wound healing in a rat model.","authors":"Marwa I Ezzat, Mai M Abdelhafez, Asmaa K Al-Mokaddem, Shahira M Ezzat","doi":"10.1007/s10787-025-01681-6","DOIUrl":"10.1007/s10787-025-01681-6","url":null,"abstract":"<p><p>The present study explores the metabolic profiling and molecular wound-healing mechanisms of Echinacea purpurea (L.) Moench (EP) flowers aqueous (AE) and ethanol (EE) extracts in an excision wound-healing model. Metabolic profiling of the extracts was investigated using UHPLC-ESI-TOF-MS and molecular networking. Antioxidant activity was carried out using the DPPH (1, 1-diphenyl-2-picrylhydrazyl) radical scavenging method and FRAP (ferric reducing antioxidant power). Carboxy methylcellulose gels of 5 and 10% of both aqueous (AE) and ethanol (EE) extracts were prepared. The wounds were explored macroscopically, histologically, and immunohistochemically. The UHPLC-ESI-TOF-MS method enabled the identification of 3 organic acids, 14 phenolic acids, 3 phenylethanoid glycosides, and 11 flavonoids from EP extracts. EE had significant antioxidant activity compared to AE. The EP treated wounds healed faster. The EE succeeded in improving healing properties and controlling the inflammatory response by reducing IL-6 and increasing IL-10 expression and enhancing angiogenesis and remodeling via increased NF-κB, TGF-β, VEGF, CD31 expression and α-SMA and collagen deposition. It is worth mentioning that the EE groups also showed improvement in the histopathological examination in a dose-dependent manner. The effectiveness of EE in wound-healing may be attributed to its higher content of polyphenols which also made the antioxidant potential of the EE and its capacity to donate electrons higher than that of AE. This study scientifically enables the understanding of the molecular mechanisms Echinacea purpurea extract in wound healing via modulating skin inflammatory response and indicates the potential usefulness of EP ethanol extract for wound healing.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2151-2164"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143572841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gallic acid enhances memory, learning and reduces neuroinflammation in a rat model of scopolamine-induced cholinergic dysfunction.","authors":"Mahbobe Alikhanzade, Maryam Khosravi, Mahmoud Hosseini, Arezoo Rajabian","doi":"10.1007/s10787-025-01699-w","DOIUrl":"10.1007/s10787-025-01699-w","url":null,"abstract":"<p><p>Gallic acid (GA), a potent polyphenol antioxidant, has demonstrated beneficial effects on the nervous system. This study aimed to investigate the neuroprotective potential of GA on learning and memory in a rat model of scopolamine-induced cholinergic dysfunction. Additionally, the roles of oxidative stress and neuroinflammation were examined. Rats were divided into six groups: Control, scopolamine (2 mg/kg/day), scopolamine plus 25, 50, or 100 mg/kg of GA, and scopolamine plus 2 mg/kg of donepezil (DN, administered once daily). Behavioral performance was evaluated using the Morris Water Maze (MWM) and Passive Avoidance Test. Biochemical parameters were assessed to determine oxidative stress, and gene expression analyses were conducted to explore neuroinflammation in the hippocampus. The behavioral tests revealed that both GA and DN treatments improved the rats' performance in the MWM, as evidenced by their ability to locate the platform and spend more time in the target area. Additionally, GA administration increased the latency of entering the dark compartment and extended the time spent in the light compartment while reducing the frequency of dark compartment entries in the Passive Avoidance Test. Furthermore, GA exhibited antioxidant, anti-acetylcholinesterase, and anti-inflammatory effects, as indicated by the modulation of malondialdehyde levels, thiol content, superoxide dismutase activity, acetylcholinesterase activity, and the expression of inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, and IL-6. In conclusion, this study provides evidence for the potential therapeutic benefits of GA in Alzheimer's disease, highlighting its ability to enhance memory function and mitigate oxidative stress, acetylcholinesterase activity, and inflammation.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2095-2108"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143647913","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":"Vanillic acid ameliorates collagen-induced arthritis by suppressing the inflammation response via inhibition of the MAPK and NF-κB signaling pathways.","authors":"Yu Zhou, Pengfei Li, Zhongwen Zhi, Rong Chen, Chenghai Li, Chunbing Zhang","doi":"10.1007/s10787-025-01645-w","DOIUrl":"10.1007/s10787-025-01645-w","url":null,"abstract":"<p><strong>Objective: </strong>To explore the potential therapeutic effects and underlying mechanism of vanillic acid (VA) in the treatment of rheumatoid arthritis (RA).</p><p><strong>Methods: </strong>A collagen-induced arthritis (CIA) model was established in DBA/1 J mice. Methotrexate (MTX, 1 mg/kg/d) and VA (5 mg/kg/d, 10 mg/kg/d, 20 mg/kg/d) were then administered to investigate their therapeutic efficacy on RA in vivo. The body weight, joint score, and spleen index of the mice in different experimental groups were evaluated. Micro-CT was performed to detect joint destruction in the mice, and HE staining was utilized to observe the pathological conditions of their joints and spleens. Quantitative real-time PCR (qRT-PCR) and enzyme linked immunosorbent assay (ELISA) were used to detect inflammatory cytokines and chemokines. Changes in synovial tissue signaling pathways were detected using immunohistochemistry. For in vitro analysis, RAW 264.7 cells were pretreated with different concentrations of VA (25, 50, 100 μg/ml) and then treated with lipopolysaccharide (LPS), and changes in their signaling pathways were detected by western blot (WB).</p><p><strong>Results: </strong>VA improved the clinical symptoms and bone destruction of arthritis in CIA mice, reduced pathological damage to ankle synovial and spleen tissue, and inhibited polarization of macrophages to M1 in the synovial tissue as well. In addition, VA inhibited the expression of TNF-α, IL-6, IL-1β, MCP-1, and iNOS in CIA mice and in LPS-stimulated RAW264.7 cells and also inhibited the phosphorylation of p65, IκBα, ERK, JNK, and p38 MAPKs.</p><p><strong>Conclusions: </strong>VA can significantly improve the clinical symptoms of RA and exerts anti-inflammatory effects by inhibiting the activation of the NF-κB/MAPK pathway.</p>","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"1949-1963"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11991997/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143440716","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editorial expression of concern: Chemomodulatory effect Melastoma Malabathricum Linn against chemically induced renal carcinogenesis rats via attenuation of inflammation, oxidative stress, and early markers of tumor expansion.","authors":"Amita Verma, Prakash Chandra Bhatt, Gaurav Kaithwas, Nikunj Sethi, Mohd Rashid, Yashwant Singh, Mahfoozur Rahman, Fahad Al-Abbasi, Firoz Anwar, Vikas Kumar","doi":"10.1007/s10787-025-01684-3","DOIUrl":"10.1007/s10787-025-01684-3","url":null,"abstract":"","PeriodicalId":13551,"journal":{"name":"Inflammopharmacology","volume":" ","pages":"2191"},"PeriodicalIF":4.6,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143482914","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}