British Journal of Pharmacology最新文献

{"title":"Dietary melatonin and its benefits on cardiovascular disease.","authors":"Karabo Tisane, Carmelita Abrahams, Sandrine Lecour","doi":"10.1111/bph.70673","DOIUrl":"https://doi.org/10.1111/bph.70673","url":null,"abstract":"<p><p>Cardiovascular disease remains the leading cause of mortality globally, with a disproportionate burden in low- and middle-income countries. Melatonin, a hormone primarily produced by the pineal gland, exhibits notable antioxidant, anti-inflammatory and immunomodulatory properties that may confer cardiovascular benefits. Importantly, melatonin is also found in a wide range of dietary sources, raising the possibility that regular consumption of melatonin-rich foods could offer a low-cost, accessible strategy to support cardiovascular health. This review summarises knowledge on dietary melatonin and evaluates its potential to provide cardiovascular benefits.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036310","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":"Repositioning niclosamide and alectinib to inhibit the hyperphosphorylation of SARS-CoV-2's nucleocapsid protein.","authors":"Song Chen, Zunyu He, Jean Kanyo, TuKiet Lam, Grace Ha, Brett Lindenbach, Ya Ha","doi":"10.1111/bph.70679","DOIUrl":"https://doi.org/10.1111/bph.70679","url":null,"abstract":"<p><strong>Background and purpose: </strong>In the past two decades, three pathogenic coronaviruses, including SARS-CoV-2, spilled over from natural animal reservoirs into the human population. Upon entry into infected cells, the nucleocapsid (N) protein of coronavirus becomes heavily phosphorylated within its central Ser-Arg domain by host kinase GSK-3, which triggers genomic RNA unpackaging and facilitates its recruitment to the replication transcription complex. Although initially considered a promising antiviral strategy, inhibiting N hyperphosphorylation requires high concentrations of kinase inhibitor and is impractical to achieve by conventional pharmacological means.</p><p><strong>Experimental approach: </strong>We investigated the effect of GSK-3 inhibition on SARS-CoV-2 replication in Calu-3 and Vero E6 cells. The dose-dependent effect of the GSK-3 inhibitor to block N hyperphosphorylation was examined in 293T cells heterologously expressing the viral protein. Liquid chromatography-tandem mass spectrometry analysis was performed to evaluate the phosphorylation profile of the purified N protein.</p><p><strong>Key results: </strong>GSK-3 inhibition delays the release of progeny virus from infected cells. N hyperphosphorylation relies on a complex, redundant priming mechanism and exhibits strong cooperativity, which together contribute to resistance against GSK-3 inhibitors. The N^R203M and N^R203K/G204R mutations-present in the delta and omicron variants of concern (VOCs), respectively-reduce the efficiency of GSK-3-mediated phosphorylation. We discovered a novel pharmacological tool combining niclosamide and alectinib that partially degrades GSK-3 and restores the sensitivity of N hyperphosphorylation to the clinically tested GSK-3 inhibitor, enzastaurin.</p><p><strong>Conclusions and implications: </strong>This work provides the biochemical basis for a novel approach to treat COVID-19 by synergistically repositioning two FDA-approved drugs.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149036312","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":"Generative AI in pharmacology publishing: Detection is necessary; governance of disclosure and equity is the harder task.","authors":"Răzvan M Cherecheș","doi":"10.1111/bph.70684","DOIUrl":"https://doi.org/10.1111/bph.70684","url":null,"abstract":"","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023953","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":"Zebrafish in the era of single-cell and spatial transcriptomics: a new paradigm for central nervous system drug discovery from natural products.","authors":"Yingyi Huang, Xiang Liu, Guangyi Fan, Guiyi Gong, Simon Ming-Yuen Lee","doi":"10.1111/bph.70662","DOIUrl":"https://doi.org/10.1111/bph.70662","url":null,"abstract":"<p><p>Natural products (NPs) represent a an important chemical source for CNS therapeutics for central nervous system (CNS) therapeutics, yet elucidating their complex, multitarget mechanisms remains a major challenge. Zebrafish have emerged as a powerful vertebrate model bridging the translational gap between in vitro assays and rodent systems in CNS drug discovery. Their genetic tractability, optical transparency and rapid development make them ideal for high-throughput pharmacological screening. Recent advances in single-cell RNA sequencing (scRNA-seq) and spatial transcriptomics (ST), particularly Stereo-seq, are revolutionizing zebrafish-based drug discovery by enabling unprecedented resolution of cellular heterogeneity, tissue architecture and drug-induced transcriptomic changes. scRNA-seq allows for the dissection of individual cellular responses, uncovering dynamic and context-specific drug effects, while Stereo-seq maps gene expression within intact tissue landscapes, offering spatial precision. When integrated, these technologies empower researchers to conduct high-resolution compound screening, elucidate mechanisms of NPs, detect off-target effects and accelerate translational pipelines from zebrafish to human models. Coupled with CRISPR-based gene editing and phenotypic assays, this integrative approach positions zebrafish as a cornerstone of modern pharmacology and a transformative platform for CNS therapeutics.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149023906","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":"EXT1 in cardiomyocytes promotes heparan sulphate-dependent accumulation of macrophage-derived SOD2 to protect against post-myocardial infarction injury.","authors":"Xie Li, Yinan Lin, Xiaozhi Xu, Yating Li, Jie Hu, Mengjie Liu, Shilin Jia, Yuru Shao, Marta Llovera, Fangrong Yan, Ruiyan Li, Yuhang Sheng, Liang Jin, Daniel Sanchis, Junmei Ye","doi":"10.1111/bph.70663","DOIUrl":"https://doi.org/10.1111/bph.70663","url":null,"abstract":"<p><strong>Background and purpose: </strong>Myocardial infarction (MI) triggers extracellular matrix (ECM) remodelling and oxidative stress, leading to cardiomyocyte injury and adverse cardiac remodelling. Heparan sulphate (HS), a major ECM component, plays an important role in regulating cell-cell communication and stress responses. Exostosin-1 (EXT1), a glycosyltransferase essential for HS biosynthesis, is highly expressed in cardiomyocytes, yet its role in post-MI repair remains incompletely understood.</p><p><strong>Experimental approach: </strong>We investigated the role of cardiomyocyte EXT1 in myocardial ischaemic injury using genetic and pharmacological approaches in vitro and in vivo.</p><p><strong>Key results: </strong>Cardiomyocyte-specific Ext1 silencing exacerbated infarct size, mitochondrial abnormalities, oxidative stress and fibrosis following permanent left anterior descending coronary artery ligation, whereas EXT1 preserved mitochondrial integrity and redox balance under hypoxic stress. Mechanistically, infiltrating macrophages released superoxide dismutase 2 (SOD2), and myocardial accumulation of macrophage-derived SOD2 was reduced after EXT1 depletion or HS disruption. HS disruption impaired SOD2 accumulation and worsened ischaemic injury, while pharmacological activation of macrophages with dimethyl itaconate (DMI) enhanced SOD2 release and conferred cardioprotection in an EXT1-dependent manner.</p><p><strong>Conclusions and implications: </strong>These findings identify cardiomyocyte EXT1 as a regulator of HS-dependent macrophage-cardiomyocyte crosstalk that limits oxidative damage and adverse remodelling after MI. They further suggest that modulation of the EXT1-HS axis, including pharmacological enhancement of macrophage antioxidant signalling by DMI, may represent a strategy to reinforce endogenous cardioprotection after ischaemic injury.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011913","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":"TRPM3 regulates fear memory encoding and seizure susceptibility in the lateral amygdala.","authors":"Attila Gyéresi, Laura Mundrucz, Máté Deák, Angéla Kecskés, Éva Borbély, Viktória Kormos, Balázs Gaszner, Orsolya Mihály, Balázs István Tóth, Joris Vriens, Thomas Voets, Erzsébet Kövesdi, Miklós Kecskés","doi":"10.1111/bph.70669","DOIUrl":"https://doi.org/10.1111/bph.70669","url":null,"abstract":"<p><strong>Background and purpose: </strong>TRPM3 is best known for its role as a peripheral sensor of pain and heat. Recent studies reporting gain-of-function TRPM3 mutations in patients with neurodevelopmental and epilepsy-associated disorders suggest a previously unrecognized role of this channel in the brain. However, the function of TRPM3 in neurons of the brain remains largely unexplored.</p><p><strong>Experimental approach: </strong>Using a battery of in vivo and in vitro electrophysiological and histological experiments, we studied the effect of TRPM3 channel on amygdala-related functions.</p><p><strong>Key results: </strong>Here, we identify TRPM3 expression in excitatory neurons of the lateral nucleus of the amygdala (LA), a brain region critical for fear learning also implicated in neuropsychiatric and epileptic disorders. We demonstrate that TRPM3 is functionally active in LA neurons and regulates their intrinsic electrophysiological properties. Consistent with this role, genetic ablation of TRPM3 in mice impairs fear memory formation. Moreover, in a kainic acid-induced epilepsy model, loss of TRPM3 reduces seizure severity, whereas pharmacological activation of the channel exacerbates seizure phenotypes. Finally, we demonstrate the presence of TRPM3 transcripts in neurons of the human LA.</p><p><strong>Conclusions and implications: </strong>Together, these findings uncover a central role for TRPM3 in amygdala function and identify this ion channel as a modulator of fear memory and seizure susceptibility.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149011861","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":"Bioengineered microbiotic levodopa therapy improves cognition and reduces pathology in a rat model of Alzheimer's disease.","authors":"Mona Abdelhamid, Piyush Padhi, Mahsa Gifani, John S Beck, Jacob P Thomas, Gargi Khadse, Catherine Kudela, Gregory J Phillips, Anumantha G Kanthasamy, Scott E Counts","doi":"10.1111/bph.70670","DOIUrl":"https://doi.org/10.1111/bph.70670","url":null,"abstract":"<p><strong>Background and purpose: </strong>Degeneration of the pontine noradrenergic and midbrain dopaminergic systems contributes to cognitive-behavioural disturbances during the prodromal stages of Alzheimer's disease (AD). We developed a genetically engineered, programmable probiotic Escherichia coli Nissle 1917 strain (EcN^rha _L-DOPA) capable of producing L-3,4-dihydroxyphenylalanine (L-DOPA) in a sustained and titratable manner, thus offering a novel gut-brain delivery mechanism to increase brain levels of noradrenaline and dopamine during the early stages of AD.</p><p><strong>Experimental approach: </strong>We replicated locus coeruleus (LC) projection system degeneration in AD by administering dopamine-β-hydroxylase IgG-saporin immunotoxin into the prefrontal cortex of 6-months-old Tg344-19 AD rats. The animals then received EcN^rha _L-DOPA/benserazide or placebo by daily gavage for 6 weeks. We assessed cognitive-behavioural function prior to postmortem assessments of amyloid-β plaque load, glial cell activation and neuronal and synaptic markers. Gut colonization, along with plasma and brain L-DOPA, dopamine, noradrenaline and metabolite levels, were also measured.</p><p><strong>Key results: </strong>EcN^rha _L-DOPA displayed stable gut colonization and resulted in sustained therapeutic levels of L-DOPA in plasma and brain, resulting in increased cortical and hippocampal noradrenaline levels. EcN^rha _L-DOPA reduced anxiety-like behaviour improved spatial and working memory. The treatment reduced forebrain Aβ plaque and MHC-II antigen-presenting microglial load. Additionally, EcN^rha _L-DOPA increased protein levels of the dendritic spine marker PSD95.</p><p><strong>Conclusions and implications: </strong>This translational study suggests that EcN^rha _L-DOPA modifies AD by boosting brain catecholamine production, reducing Aβ accumulation and neuroinflammation, promoting synaptic health, and enhancing cognitive function. Collectively, these results highlight EcN^rha _L-DOPA as a promising preclinical engineered gut microbiome-based therapeutic strategy for early-stage AD.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001262","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":"Natural product-derived TRPM7 channel inhibitors in neurological injury: Mechanisms, pharmacological potential and translational challenges.","authors":"Xinyang Zhang, Hio Lam Ho, F David Horgen, Andrea Fleig, Zhong-Ping Feng, Hong-Shuo Sun","doi":"10.1111/bph.70667","DOIUrl":"https://doi.org/10.1111/bph.70667","url":null,"abstract":"<p><p>Disruption of intracellular ionic homeostasis is a convergent pathological feature across diverse neurological injuries and disorders, including ischaemic and haemorrhagic stroke, hypoxic-ischaemic brain injury, traumatic brain injury, epilepsy and brain tumour. Among stress-activated ion channels implicated in these conditions, the transient receptor potential melastatin 7 (TRPM7) channel has emerged as a key mediator linking metabolic stress to sustained dysregulation of Ca²⁺, Mg²⁺ and Zn²⁺ signalling and downstream injury cascades. TRPM7 is a unique bifunctional protein composed of a divalent cation-permeable ion channel fused with a C-terminal α-kinase domain, enabling integration of ionic flux with intracellular signalling. Accumulating evidence from cellular, electrophysiological and in vivo studies demonstrates that TRPM7 contributes causally to neuronal injury, vascular dysfunction, network hyperexcitability and tumour cell malignancy across disease models. Natural products have historically played a central role in ion channel pharmacology, and growing evidence has identified structurally diverse natural product-derived compounds as modulators of TRPM7 channel. In this review, we synthesize mechanistic and pharmacological evidence supporting TRPM7 as a tractable therapeutic target, with particular focus on representative natural product-derived TRPM7 channel inhibitors including carvacrol, waixenicin A and xyloketal B, which span a spectrum of potency, selectivity and mechanistic complexity. We further discuss key translational challenges associated with targeting TRPM7 in neurological injury, including target selectivity, essential physiological roles, CNS exposure and context-dependent disease effects. Collectively, available evidence positions TRPM7 as a pharmacologically actionable target and highlights the potential of natural product scaffolds to guide the development of next-generation TRPM7-directed therapies for neurological injury.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149001301","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":"Alamandine/MrgD pathway modulates gut-bone marrow axis in ageing.","authors":"Kishore Chittimalli, Henryata E Rozario, Victor Martinez, Zachary L McAdams, Stephen A Adkins, Aaron C Ericsson, Yagna P R Jarajapu","doi":"10.1111/bph.70656","DOIUrl":"10.1111/bph.70656","url":null,"abstract":"<p><strong>Background and purpose: </strong>Ageing is associated with colon epithelial barrier disruption and up-regulation of myelopoiesis in the bone marrow (BM). Alamandine (Ala) and MrgD are novel members of the renin angiotensin system (RAS). This study tested the hypothesis that Ala restores the colon epithelial barrier integrity in ageing via modulating gut-BM axis.</p><p><strong>Experimental approach: </strong>Mice, 2-3 (Young) or 22-24 months (Old), were treated with saline or Ala by using Osmotic pumps. The intestinal permeability was evaluated using FITC-dextran. Lgr5⁺Olfm4⁺ intestinal stem cells (ISCs), Wnt3a and β-catenin were evaluated by immunohistochemistry or western blotting. Faecal microbiome was analysed by 16S rRNA sequencing. Monocyte-macrophages were characterized by flow cytometry. Caecal or serum bacterial metabolites were analysed and the caecal supernatants (CS) were tested for myelopoietic potential.</p><p><strong>Key results: </strong>MrgD was expressed in ISCs, which was decreased in the Old. Increased intestinal permeability in ageing was reversed by Ala. In the colon organoids, Ala increased Wnt3a levels and this was antagonized by NF449, SQ22536 or 666-15. Ala restored phospho-CREB and active β-catenin levels that were decreased in the Old colon-organoids. Ala increased the richness and β-diversity of the microbiota with decreased Bacillota/Bacteroidota in ageing. Ala decreased the CD80⁺ and increased CX3CR⁺ macrophages in the Old colons. Old-CS induced myelopoiesis in BM cells with higher number of pro-inflammatory macrophages, which was prevented by Ala treatment.</p><p><strong>Conclusions and implications: </strong>Targeting Ala/MrgD pathway is a promising approach for ameliorating the inflammatory stress in ageing by restoring homeostasis in the gut-BM inter-organ communication.</p>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":" ","pages":""},"PeriodicalIF":7.5,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982327","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":"Kinase Inhibitor Cardiotoxicity Database (KICDB): a causality-oriented multi-omics database for kinase inhibitor-induced cardiotoxicity","authors":"Jiamin Wei,&nbsp;Yin Liu,&nbsp;Miaoqing Wu,&nbsp;Guoyuan Li,&nbsp;Xinyao Zheng,&nbsp;Huafeng Fu,&nbsp;Jian Zhang,&nbsp;Jijin Lin","doi":"10.1111/bph.70599","DOIUrl":"10.1111/bph.70599","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 <h3> Background</h3>\u0000 \u0000 <p>Kinase inhibitors (KIs) are essential in targeted cancer therapy but frequently cause cardiotoxicity, limiting their clinical utility. A systematic resource to explore the underlying causal mechanisms is urgently needed.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Methods</h3>\u0000 \u0000 <p>We developed the Kinase Inhibitor Cardiotoxicity Database (KICDB ), an interactive web platform integrating large-scale transcriptomic meta-analysis with causal inference to identify molecular determinants of KI-induced cardiotoxicity.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Results</h3>\u0000 \u0000 <p>Meta-analysis of 5291 samples revealed a convergent disruption of the cellular mitotic machinery, specifically chromosome segregation and nuclear division, as a shared mechanism of toxicity across multiple KI classes. Furthermore, Mendelian randomization (MR) analysis identified 26 robust causal associations, linking specific kinase targets (e.g. RING finger protein 13 [RNF13] and tyrosine kinase with immunoglobulin like and EGF like domains 1 [TIE1]) to increased risks of cardiomyopathy and myocardial infarction, while identifying TYRO3 protein tyrosine kinase [Tyro3] and Janus kinase 2 (JAK2) as potential cardioprotective factors.</p>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Conclusions</h3>\u0000 \u0000 <p>KICDB provides a mechanistic framework linking transcriptomic perturbations with genetically validated causal drivers. By linking transcriptomic perturbations with causal validation, it serves as a resource to advance biomarker discovery, mechanistic exploration and the design of cardioprotective strategies.</p>\u0000 </section>\u0000 </div>","PeriodicalId":9262,"journal":{"name":"British Journal of Pharmacology","volume":"183 20","pages":"6046-6058"},"PeriodicalIF":7.5,"publicationDate":"2026-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148469171","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}