Clinical science最新文献

{"title":"Blood Pressure Reduction and Anti-inflammatory Macrophage Augmentation Attenuate Uterine Immune Dysregulation and Inflammation in Mice with Salt-Sensitive Hypertension.","authors":"Shobana Navaneethabalakrishnan, Bethany L Goodlett, Hannah L Smith, Alyssa Cardenas, Robert A Montalvo, Gabriella C Peterson, Brett M Mitchell","doi":"10.1042/CS20255879","DOIUrl":"https://doi.org/10.1042/CS20255879","url":null,"abstract":"<p><p>Salt-sensitive hypertension (SSHTN) promotes systemic inflammation, pro-inflammatory immune cell infiltration, and end-organ damage, including in the kidneys and gonads. However, its impact on uterine immune cell populations remains unclear. We hypothesized that SSHTN alters immune cell homeostasis, induces inflammation, and promotes lymphangiogenesis in the uterus, and that these effects can be mitigated by pharmacological blood pressure (BP) reduction and anti-inflammatory macrophage augmentation. To test the hypothesis, female C57BL6/J mice were given nitro-L-arginine methyl ester hydrochloride (L-NAME; 0.5 mg/mL) in drinking water for 2 weeks, followed by a 2-week washout period. Mice were then subjected to 4% high salt diet (SSHTN) for 3 weeks. Another group of mice received either hydralazine (HYD; 250 mg/L in drinking water), a vasodilator (SSHTN+HYD), or AVE0991 (0.58 μmol/kg body weight/day), a non-peptide Mas receptor agonist, through daily intraperitoneal injections (SSHTN+AVE). Control mice received tap water and a standard diet for the entire treatment period. Flow cytometry data revealed a significant decrease in total uterine CD45+ immune cells, along with an increase in tissue macrophages, in all SSHTN groups compared to the control group. SSHTN mice had increased uterine pro-inflammatory macrophages, dendritic cells, natural killer cells, and CD4⁺ pro-inflammatory T cells, all of which were mitigated by HYD and AVE0991 treatments. SSHTN promoted uterine inflammation, lymphatic vessel expansion, and altered hormone receptor expression, which were mitigated by pharmacological intervention, highlighting their therapeutic potential in preserving uterine homeostasis and improving reproductive health in women with SSHTN.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238094","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":"Macrophage plasticity and glucose metabolism: the role of immunometabolism in pulmonary arterial hypertension.","authors":"Lindsay Jefferson, Patricia D A Lima, Stephen L Archer","doi":"10.1042/CS20257363","DOIUrl":"https://doi.org/10.1042/CS20257363","url":null,"abstract":"<p><p>Pulmonary arterial hypertension (PAH) is a syndrome characterized by a mean pulmonary artery pressure >20 mmHg and elevated pulmonary vascular resistance >2 Wood Units in the absence of left heart disease, chronic lung disease or hypoxia, and chronic thromboembolic disease. PAH is an obliterative pulmonary arteriopathy that leads to morbidity and mortality, often due to right ventricular failure (RVF). Emerging evidence from preclinical research, using chemical inhibition or genetic depletion of inflammatory mediators, reveals a role for inflammation in the adverse pulmonary vascular remodelling in PAH. More recently, studies have also identified inflammation of the right ventricle (RV) as a potential contributor to RV decompensation and failure. While inflammation contributes to the pathogenesis of PAH, no approved PH-targeted therapies specifically target inflammation. Macrophages are myeloid cells that play a critical role in inflammation and PAH. Their cellular plasticity enables the acquisition of tissue-specific phenotypes and functions that may promote either resolution or exacerbation of inflammatory signalling. Macrophage plasticity in PAH is poorly understood. We examine how alterations in glucose metabolism, particularly the uncoupling of glycolysis from glucose oxidation-a notable feature of PAH observed in various cell populations-impact macrophage polarization and the inflammatory phenotype associated with PAH. The study of immune cell metabolism, known as immunometabolism, is an emerging field that has yet to be explored in PAH. Improving understanding of the inflammatory mechanisms in PAH, particularly novel pathways related to macrophage immunometabolism, may identify new targets for anti-inflammatory therapies for PAH.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"138 19","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205860","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":"Role of conventional dendritic cells in schistosomiasis-induced pulmonary hypertension.","authors":"Claudia Mickael, Rahul Kumar, Dara C Fonseca Balladares, Kevin Nolan, Michael H Lee, Biruk Kassa, Thais C F Menezes, Anthony Lau-Xiao, Ajaypal Sahota, Linda Sanders, Katie Tuscan, Aneta Gandjeva, Kelly M Cautivo, Ari Molofsky, Brian B Graham","doi":"10.1042/CS20256896","DOIUrl":"https://doi.org/10.1042/CS20256896","url":null,"abstract":"<p><strong>Background: </strong>Schistosomiasis is a major cause of pulmonary hypertension (PH) worldwide, and CD4 T cells are critical in disease pathogenesis. The role of dendritic cells (DCs) in Schistosoma-induced PH (SchPH) is unknown. There are two types of conventional DCs, cDC1 and cDC2, that prototypically activate CD8 and CD4 T cells, respectively.</p><p><strong>Methods: </strong>We exposed wildtype, DC reporter, and DC knockout mice to Schistosoma mansoni and quantified PH severity by heart catheterization and cell density by flow cytometry.</p><p><strong>Results: </strong>Experimental S. mansoni exposure increased the density of pulmonary DCs, particularly cDC2s. Deleting both cDC subsets did not significantly modify SchPH disease severity. Deleting only cDC1s caused more severe SchPH, associated with more Th2 CD4 and CD8 T cells. In contrast, deleting only cDC2s reduced SchPH disease severity.</p><p><strong>Conclusions: </strong>cDC1s appear to be protective, whereas cDC2s promote disease in SchPH.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145238194","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":"Physiological roles of phosphoinositides and inositol phosphates: Implications for metabolic dysfunction-associated steatotic liver disease.","authors":"Zhili Cheng, Magdalene K Montgomery","doi":"10.1042/CS20257631","DOIUrl":"https://doi.org/10.1042/CS20257631","url":null,"abstract":"<p><p>Phosphoinositides and inositol phosphates (IPs) are integral to numerous cellular processes, including membrane trafficking, signal transduction and calcium dynamics. These lipid-derived signalling mediators orchestrate the spatial and temporal regulation of many signalling cascades, largely through interactions with specific effector proteins. Recent studies have highlighted their critical roles in metabolic homeostasis and the pathogenesis of metabolic dysfunction-associated steatotic liver disease (MASLD). In this review, we examine the pathways important for phosphoinositide and IP synthesis, and the physiological functions of myo-inositol, d-chiro-inositol and phosphatidylinositol, as well as their phosphorylated inositol counterparts, including phosphoinositides (PI(3)P, PI(4)P, PI(3,4)P2, PI(3,5)P2, PI(4,5)P2, PI(3,4,5)P3) and IPs (inositol 1,4,5-trisphosphate (IP3), inositol 1,3,4,5-tetrakisphosphate (IP4), inositol pentakisphosphate (IP5), inositol hexaphosphate (IP6 or phytic acid) and inositol pyrophosphates (IP7 and IP8)), with an emphasis on their emerging significance in hepatic metabolism. We explore how perturbations in IP metabolism contribute to the development and progression of MASLD, liver inflammation, fibrosis and hepatic insulin resistance. We further highlight recent studies utilizing genetic models and pharmacological interventions that underscore the therapeutic potential of targeting inositol metabolism in MASLD. This review synthesizes current knowledge to provide a comprehensive understanding of how phosphoinositides and IPs integrate metabolic cues and contribute to hepatic pathophysiology, identifying knowledge gaps and offering novel insights for therapeutic innovation in the management of MASLD.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 19","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145205801","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":"Double-edged mitophagy: balancing inflammation and resolution in lung disease.","authors":"Sijia Tian, Yingyi Zhang, Chuanchuan Liu, Huajing Zhang, Qianying Lu, Yanmei Zhao, Haojun Fan","doi":"10.1042/CS20256705","DOIUrl":"https://doi.org/10.1042/CS20256705","url":null,"abstract":"<p><p>Inflammatory lung diseases, such as chronic obstructive pulmonary disease (COPD), acute lung injury (ALI)/acute respiratory distress syndrome (ARDS), and asthma, are driven by mitochondrial dysfunction and aberrant immune responses, yet the regulatory role of mitophagy-a selective autophagy eliminating damaged mitochondria-remains poorly defined. This review synthesizes evidence from in vivo and in vitro studies to dissect the molecular interplay between mitophagy and inflammation. Key fundings reveal that mitophagy exerts context-dependent effects: Protective mitophagy (via PTEN-induced putative kinase 1 [PINK1]-Parkin or FUN14 domain-containing protein 1 [FUNDC1] pathways) clears mitochondrial reactive oxygen species (mtROS)/mitochondrial DNA (mtDNA), suppressing NOD-like receptor thermal protein domain associated protein 3 (NLRP3) inflammasome activation and pyroptosis, but excessive mitophagy exacerbates mitochondrial fragmentation and necroptosis. Notably, bidirectional cross-talk exists, and therapeutic strategies-genetic and pharmacological-could restore mitophagy flux, attenuating inflammation in preclinical models. However, challenges persist in targeting tissue-specific mitophagy (such as alveolar and bronchial epithelia). This work underscores mitophagy as a double-edged sword in lung inflammation and proposes precision interventions to balance mitochondrial quality control, offering novel avenues for inflammatory lung diseases.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 19","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145198316","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":"Physiological response to fetal intravenous lipid emulsion in mid-gestation.","authors":"Neeka Barooni, Athena Chen, Sarah M Alaniz, Jessica Minnier, Samantha Louey, Sonnet S Jonker","doi":"10.1042/CS20256946","DOIUrl":"10.1042/CS20256946","url":null,"abstract":"<p><p>Circulating lipid levels are typically low in fetuses, and exposure to high lipid levels at developmental stages prior to term birth is sometimes associated with pathology. Experimentally, near-term fetuses tolerate one week of high lipid concentrations; it is unknown whether this brief exposure to elevated circulating lipids is pathological at an earlier developmental age. We studied the physiological response to intravenous lipid emulsion during mid-gestation. Fetal sheep received intravenous Intralipid 20® (n = 9) or Lactated Ringer's Solution (n = 8) from 85.0 ± 0.7 to 97.0 ± 0.7 days of gestation (term = 147 days). Intralipid was administered according to manufacturer's recommendations, with an initial dose of 0.5-1 g/kg/d that increased daily to a maximum of 3 g/kg/d. Hemodynamic and arterial blood parameters were assessed throughout the study. Fetal growth, liver function, and lipid droplet accumulation were measured on the final day. Fetal hemodynamics and blood gases did not change as a result of the treatment. Compared with Controls, Intralipid fetuses had lower blood lactate concentrations (1.3 ± 0.2 vs. 1.0 ± 0.2 mmol/l, P=0.009) after eight days of treatment. Conjugated (0.4 ± 0.1 vs. 0.6±0.1 mg/dl, P<0.001) and unconjugated (0.3 ± 0.1 vs. 1.2 ± 0.5 mg/dl, P<0.001) bilirubin levels were higher in Intralipid-infused fetuses than in Controls. Fetal somatic growth was unchanged, but heart weight was lower in fetuses receiving Intralipid (6.9 ± 0.7 vs. 6.1±0.7 g, P=0.008). Compared with Controls, Oil Red O staining was elevated in the liver and heart of Intralipid-infused fetuses (liver score: 18.9 ± 17.2 vs. 371.7±44.2, P<0.0001; heart score: 1.8 ± 2.8 vs. 97.6 ± 60.1, P=0.0006). Our findings suggest that mid-gestation fetal sheep can tolerate intravenous lipid emulsion. Lipid accumulation in the liver and heart may precede pathologies associated with ectopic lipid storage, but further research is needed to understand the long-term consequences of Intralipid infusion at this developmental stage.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":"997-1013"},"PeriodicalIF":7.7,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12456272/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144945408","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":"TSPAN4 controls vascular smooth muscle cell phenotypic switching and intimal hyperplasia by targeting TPM1-regulated cytoskeletal organization.","authors":"Shengbiao Li, Kexin Chen, Yi Zhang, Yang Yu, Tianyi Zhang, Donghui Jiang, Mi Li, Shubo Fu, Ji Chen, Jiapan Li, Jingyan Yi, Rong Li, Gan Qiao, Jianguo Feng, Jun Jiang, Qiong Yuan, Chunxiang Zhang","doi":"10.1042/CS20255833","DOIUrl":"https://doi.org/10.1042/CS20255833","url":null,"abstract":"<p><p>Vascular smooth muscle cell (VSMC) phenotypic switching, followed by enhanced proliferation and migration, is a key event in the development of intimal hyperplasia in diverse vascular diseases. While tetranspanin 4 (TSPAN4) is known to be expressed in the vasculature, its function in VSMC phenotypic switching and vascular disease is currently unknown. Here, we investigated the role of TSPAN4 using an in vitro model of PDGF-BB-induced phenotypic switching and an in vivo carotid artery ligation model in wild-type and TSPAN4-deficient mice. Our experiments, including EdU assays, Transwell assays, western blot analysis, and immunoprecipitation, revealed that TSPAN4 expression is elevated in human atherosclerotic arteries, ligated mouse carotid arteries, and PDGF-BB-stimulated VSMCs. Additionally, TSPAN4 overexpression promoted the switch from a contractile to a synthetic phenotype, accompanied by enhanced VSMC proliferation and migration. Conversely, TSPAN4 knockdown inhibited these effects, suppressing PDGF-BB-induced phenotypic switching. Mechanistically, TSPAN4 was found to interact with and influence the expression and localization of tropomyosin-1 (TPM1). This, in turn, impacted cytoskeletal organization, ultimately driving phenotypic switching and functional alterations in VSMCs. Finally, we demonstrated that TSPAN4 deficiency in mice attenuated vascular neointimal formation following carotid artery ligation. These findings suggested that TSPAN4 is a promising novel therapeutic target for vascular remodeling and proliferative vascular diseases.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145148010","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":"Evaluating the role of 2-hydroxyestradiol in modulating TNF-α signaling and its implications in rheumatoid arthritis.","authors":"Prachi Agnihotri, Mohd Saquib, Ajit Kumar, Lovely Joshi, Debolina Chakraborty, Ashish Sarkar, Vijay Kumar, Sagarika Biswas","doi":"10.1042/CS20241917","DOIUrl":"https://doi.org/10.1042/CS20241917","url":null,"abstract":"","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 18","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124629","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":"The physiology of MASLD: molecular pathways between liver and adipose tissues.","authors":"Wang-Hsin Lee, Zachary A Kipp, Evelyn A Bates, Sally N Pauss, Genesee J Martinez, Terry D Hinds","doi":"10.1042/CS20257571","DOIUrl":"https://doi.org/10.1042/CS20257571","url":null,"abstract":"<p><p>The global prevalence of obesity has exerted a profound influence on human health. It has contributed to numerous obesity-related comorbidities, including metabolic dysfunction-associated steatotic liver disease (MASLD) and insulin-resistant diabetes. MASLD is diagnosed when there is substantial fat accumulation concomitant with five additional diagnostic criteria. If untreated, MASLD may progress to liver fibrosis and cirrhosis, conditions that can be life-threatening in the final stages. Nonetheless, the development and progression of MASLD are complex, and its underlying mechanisms remain incompletely elucidated. Typically, during fasting, adipose tissue releases fatty acids, which the liver subsequently uptakes for gluconeogenesis. However, this process, along with many others, is impaired in the liver and adipose tissue of individuals with MASLD. This review provides comprehensive details on the mechanisms underlying adiposity and insulin resistance associated with MASLD. We discuss the canonical pathways that promote lipogenesis and insulin sensitivity in the liver and adipose tissues, including bile acids, bilirubin, fatty acids, inflammation, de novo lipogenesis, oxidative stress, peroxisome proliferator-activated receptors (PPARs), fibroblast growth factor 21 (FGF21), glucagon-like peptide 1 (GLP1), and metabolism of fructose. The scope of the review is expanded to encompass biological responses to fasting and feeding, as well as their effects on fat accumulation and insulin sensitivity in these tissues. Additionally, the review elaborates on critical molecular mechanisms regulating MASLD progression, including hepatic insulin clearance, insulin degradation, bilirubin metabolism, nerve innervation, and the roles of cytokines and adipokines. Overall, this review examines the mechanisms driving MASLD and explores potential novel therapeutic strategies for its management.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":"139 18","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145124638","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":"SUL-138 mitigates accelerated endothelial aging and protects the kidney.","authors":"Annika A Jüttner, Sabrina Ribeiro Gonsalez, Martijn van Heugten, Ehsan Ataei Ataabadi, Keivan Golshiri, Ewout J Hoorn, Marian Clahsen-van Groningen, Rene de Vries, Ingrid M Garrelds, Dennis Schutter, A H Jan Danser, Adrianus C van der Graaf, Daniël H Swart, Leo E Deelman, Robert H Henning, Jenny A Visser, Guido Krenning, Anton J M Roks","doi":"10.1042/CS20255735","DOIUrl":"https://doi.org/10.1042/CS20255735","url":null,"abstract":"<p><p>Vascular aging is marked by increased levels of reactive oxygen species in endothelial cells. Reactive oxygen species can amongst others be produced by dysfunctional mitochondria, contributing to acceleration of vascular aging by promoting DNA damage response and senescence. In the aged vasculature impaired endothelial cell function causes decreased vasodilation which may also have an impact on peripheral organs such as the kidney. The aim of this study was to investigate the effect of chronic treatment with SUL-138 (30 mg/kg/day), a novel mitochondrial protective compound, on DNA damage-prompted, accelerated endothelial aging and associated kidney dysfunction in mice. Endothelial-specific aging was induced by knock-out of DNA repair endonuclease Ercc1 in mice (EC-KO mice). We showed that impaired endothelium-dependent vasodilation and expression of DNA damage response markers in EC-KO mice were restored after the treatment with SUL-138. The underlying mechanism of improved vasodilation was an increase in endothelium-derived hyperpolarization (EDH). Endothelial-specific aging induced tubular injury, sodium-wasting, and increased inflammatory markers in the kidney which were normalized by the treatment with SUL-138. We conclude that accelerated endothelial aging adversely affects vascular function and causes kidney tubular injury. SUL-138 rescues endothelial aging, restores vasodilation by increasing EDH, and protects the kidney. Thus, preservation of mitochondrial function is a potential pharmacotherapeutic target in aging-related dysfunction provoked by the DNA damage response.</p>","PeriodicalId":10475,"journal":{"name":"Clinical science","volume":" ","pages":""},"PeriodicalIF":7.7,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147988","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}