npj aging最新文献_第4页

LncRNA Lncbate1 promotes lipid synthesis in the white adipose tissue during aging by targeting the miR-455-5p-ACSS1 axis. LncRNA lnbate1通过靶向miR-455-5p-ACSS1轴促进衰老过程中白色脂肪组织的脂质合成。

IF 13

npj aging Pub Date : 2026-06-19 DOI: 10.1038/s41514-026-00337-1

Jing Chen, Ning Yang, Yifan Zhang, Qianqian Yao, Chengfu Yuan

引用次数: 0

Mortality associated biological age improves independently of weight loss after bariatric surgery. 与生物年龄相关的死亡率与减肥手术后体重减轻无关。

IF 13

npj aging Pub Date : 2026-06-19 DOI: 10.1038/s41514-026-00429-y

Katharina Helena Morawitz, Wolfgang Pommer, Oleg Tsuprykov, Hendrik Krautschneider, Swantje von Germar, Nina Patzke, Felix Grassmann

{"title":"Mortality associated biological age improves independently of weight loss after bariatric surgery.","authors":"Katharina Helena Morawitz, Wolfgang Pommer, Oleg Tsuprykov, Hendrik Krautschneider, Swantje von Germar, Nina Patzke, Felix Grassmann","doi":"10.1038/s41514-026-00429-y","DOIUrl":"10.1038/s41514-026-00429-y","url":null,"abstract":"Obesity increases the risk of common diseases and mortality, placing a significant burden on our aging society. Bariatric surgery results in significant weight loss; however, the amount of associated health gain is currently less studied, particularly in the first two years. We modelled mortality-associated biological age according to established blood markers in a prospective cohort of 505 patients that underwent bariatric surgery. The difference between biological age and chronological age (age acceleration) as a molecular marker of health gain was evaluated at different time points with mixed effects models. At baseline, biological age acceleration was positively correlated to higher smoking exposure as well as increased body mass, particularly in males. Twelve months after surgery, patients were on average 5.55 years younger (slope and 95% confidence intervals (95% CI): -5.55 [-6.12; -4.97]) which remained stable until 24 months. When adjusted for changes in body mass index over time, the effect seizes decreased to 3.32 years younger age at 12 months post-surgery (slope and 95% CI: -3.32 [-4.26; -2.37]), indicating an age-rejuvenating effect - more pronounced in men - beyond weight loss. Individual markers such as glucose and C-reactive protein levels as well as blood cell counts contributing to biological age computation showed a generally more favorable change after surgery. In conclusion, biological age was markedly reduced in patients undergoing bariatric surgery resulting in a 40-50% reduction in expected mortality after two years, particularly in men. Our findings support the use of biological age as a clinically meaningful, patient-centered marker of treatment success after bariatric surgery.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":"12 1","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13280343/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148280535","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Uncovering senescent fibroblast heterogeneity connects DNA damage response to idiopathic pulmonary fibrosis. 揭示衰老成纤维细胞异质性将DNA损伤反应与特发性肺纤维化联系起来。

IF 13

npj aging Pub Date : 2026-06-18 DOI: 10.1038/s41514-026-00388-4

Jun-Wei B Hughes, Akshay Pujari, Anja Sandholm, Duncan Croll, Lea Baskin Monk, Isaac Joshua, Rachel Butterfield, Corrigan Horton, Kevin Schneider, Fiona Senchyna, Ian Brown, Zhixin A Zhang, Ana L Coelho, Tsung-Che Ho, Hideto Deguchi, Ryo Higuchi-Sanabria, Claude Jourdan Le Saux, Stefanie Deinhardt-Emmer, Lisa M Ellerby, Alberto C Vitari, David Furman, Cory M Hogaboam, Alex Laslavic, Pierre-Yves Desprez, Marco Quarta, Judith Campisi

{"title":"Uncovering senescent fibroblast heterogeneity connects DNA damage response to idiopathic pulmonary fibrosis.","authors":"Jun-Wei B Hughes, Akshay Pujari, Anja Sandholm, Duncan Croll, Lea Baskin Monk, Isaac Joshua, Rachel Butterfield, Corrigan Horton, Kevin Schneider, Fiona Senchyna, Ian Brown, Zhixin A Zhang, Ana L Coelho, Tsung-Che Ho, Hideto Deguchi, Ryo Higuchi-Sanabria, Claude Jourdan Le Saux, Stefanie Deinhardt-Emmer, Lisa M Ellerby, Alberto C Vitari, David Furman, Cory M Hogaboam, Alex Laslavic, Pierre-Yves Desprez, Marco Quarta, Judith Campisi","doi":"10.1038/s41514-026-00388-4","DOIUrl":"10.1038/s41514-026-00388-4","url":null,"abstract":"Cellular senescence is a highly heterogeneous state of cell stress response that deleteriously accumulates with age and contributes to age-related dysfunction. While the heterogeneity across cell types is well documented, variation within the same cell type is only beginning to be understood. Here, we show primary human lung fibroblasts from either donors who are healthy or diagnosed with idiopathic pulmonary fibrosis (IPF) exhibit a subtle form of heterogeneity over time after DNA damage. Moreover, senescent IPF lung fibroblasts display a dysregulated transcriptional-protein DNA damage response (DDR). Weighted gene correlation network analysis (WGCNA) reveals unique and known targets linking senescent IPF lung fibroblast heterogeneity to genes associated with DNA damage and repair and cytokine and chemokine responses. We combine our healthy and IPF senescent gene expression datasets to develop a novel gene signature of senescence-associated genes that identify disease-relevant cells in human single-cell RNA-seq (scRNA-seq) data. Collectively, our results uncover human-relevant senescence signatures, highlight IPF-specific DDR, cytokine, and chemokine targets, and expand our understanding of how a dysregulated DDR contributes to senescent cell heterogeneity in IPF.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148280546","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Inferring accumulation times of mitochondrial DNA deletion mutants from cross-sectional single-cell data: methodological framework and validation. 从横断面单细胞数据推断线粒体DNA缺失突变的积累时间：方法框架和验证。

IF 13

npj aging Pub Date : 2026-06-16 DOI: 10.1038/s41514-026-00431-4

Axel Kowald, Thomas B L Kirkwood

{"title":"Inferring accumulation times of mitochondrial DNA deletion mutants from cross-sectional single-cell data: methodological framework and validation.","authors":"Axel Kowald, Thomas B L Kirkwood","doi":"10.1038/s41514-026-00431-4","DOIUrl":"10.1038/s41514-026-00431-4","url":null,"abstract":"The accumulation of mitochondrial DNA (mtDNA) deletion mutants in post-mitotic cells is a hallmark of mammalian ageing and a key contributor to tissue decline in skeletal muscle and neurons. A transcription-coupled replication model predicts that deletions affecting a negative feedback mechanism gain a selective replication advantage, leading to relatively short accumulation times for mutant takeover. However, these accumulation times are experimentally inaccessible since single-cell measurements are destructive. Here, we present a framework to infer such accumulation times from cross-sectional single-cell RNA sequencing (scRNAseq) data, exploiting the fact that mtDNA deletions are also reflected at the transcript level. To establish feasibility, we generated synthetic datasets using two stochastic models of the mitochondrial life cycle and used these as a gold standard. We then applied the Moran process, a stochastic birth-death model, to calculate distributions of accumulation times and to extract key parameters. The Moran model reproduced the distributions obtained from stochastic simulations with high fidelity across different assumptions about mitochondrial regulation. Fitting the model to synthetic data, successfully recovered mutation probability, selection advantage, and the fraction of advantageous mutants. These results establish a methodological framework for quantifying mtDNA mutant dynamics from single-cell transcriptomic data and provide a foundation for analysing large experimental datasets in ageing research.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":"12 1","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13272806/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148267511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Age- and Sex-specific Prevalence, Longitudinal Trends and Factors of Cardiovascular-Kidney-Metabolic Syndrome Stages among Chinese Adults. 中国成人心血管-肾-代谢综合征的年龄和性别特异性患病率、纵向趋势和分期因素

IF 13

npj aging Pub Date : 2026-06-16 DOI: 10.1038/s41514-026-00428-z

Zhiyue Liang, Shiyuan Wei, Qi Gao, Shengli An, Licong Su

引用次数: 0

Network-informed multi-trait genomic analysis decodes the shared genetic architecture and therapeutic landscape of pelvic floor disorders. 网络信息多性状基因组分析解码共享遗传结构和盆底疾病的治疗景观。

IF 13

npj aging Pub Date : 2026-06-15 DOI: 10.1038/s41514-026-00430-5

Jiawen Wang, Yupeng Chen, Lingfeng Meng, Ruijie Yao, Jiong Zhang, Qingguo Zhu, Jinfeng Wu, Liefu Ye, Yaoguang Zhang

{"title":"Network-informed multi-trait genomic analysis decodes the shared genetic architecture and therapeutic landscape of pelvic floor disorders.","authors":"Jiawen Wang, Yupeng Chen, Lingfeng Meng, Ruijie Yao, Jiong Zhang, Qingguo Zhu, Jinfeng Wu, Liefu Ye, Yaoguang Zhang","doi":"10.1038/s41514-026-00430-5","DOIUrl":"10.1038/s41514-026-00430-5","url":null,"abstract":"Pelvic floor disorders, including pelvic organ prolapse and urinary incontinence, represent a common health burden with substantial clinical comorbidity, but their shared genetic architecture remains incompletely understood. We performed a multi-trait genomic analysis of six pelvic-floor-related phenotypes using publicly available GWAS summary statistics from FinnGen R12 and the GWAS Catalog, with Pan-UKBB summary statistics used only for cross-ancestry validation. Linkage disequilibrium score regression and Genomic Structural Equation Modeling identified two broad latent genetic dimensions: a structural factor related to anatomical prolapse and a functional factor related to urinary and bowel dysfunction. MAGMA gene-based analysis identified 267 significant genes enriched for extracellular matrix organization and urogenital developmental pathways, including WNT4, LOXL1, ESR1, WT1, HNF1B, and FGFR2. An exploratory network-informed machine-learning framework incorporating protein-protein interaction topology improved gene prioritization over a baseline Random Forest model and highlighted biologically plausible hub genes. Cross-ancestry analysis of Pan-UKBB female genital prolapse supported directional portability of European-discovered signals and identified WNT4 as a directionally concordant locus. These findings provide a systems-level map of pelvic-floor-related genetic architecture and prioritize candidate genes for future functional validation.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13631281/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148261060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Low circulating adropin concentrations identify vulnerability in learning-dependent cognitive performance in aged rhesus macaques. 低循环adropin浓度确定了老年恒河猴学习依赖认知表现的脆弱性。

IF 13

npj aging Pub Date : 2026-06-10 DOI: 10.1038/s41514-026-00426-1

Andrew A Butler, James L Graham, Lesly C Ceniceros, Ashlee M Cruz, Ashley D Cunningham, Riya Subedi, Anthony P Brown, Nicholas Dai, Giovanne B Diniz, Peter J Havel, John H Morrison, Erin L Kinnally

{"title":"Low circulating adropin concentrations identify vulnerability in learning-dependent cognitive performance in aged rhesus macaques.","authors":"Andrew A Butler, James L Graham, Lesly C Ceniceros, Ashlee M Cruz, Ashley D Cunningham, Riya Subedi, Anthony P Brown, Nicholas Dai, Giovanne B Diniz, Peter J Havel, John H Morrison, Erin L Kinnally","doi":"10.1038/s41514-026-00426-1","DOIUrl":"10.1038/s41514-026-00426-1","url":null,"abstract":"Identifying biomarkers that identify vulnerability to age-related cognitive decline is a major priority in aging research. Adropin, a circulating peptide that regulates metabolic and vascular homeostasis, has been associated with cognitive performance in humans, but its relevance across species has remained unclear. Here we report low plasma adropin concentrations associate with poor decision-making in aged rhesus macaques subject to an increasing food choice test paradigm. Animals with higher adropin levels exhibited faster improvement in reaction time and reductions of variability in reaction time, whereas intrinsic performance on simple tasks was preserved. These associations were most apparent under conditions requiring adaptation to novelty or stress, suggesting that adropin may signal cognitive resilience rather than baseline executive capacity. The findings parallel mechanistic data from rodent models linking adropin signaling to mitochondrial function, resistance to oxidative stress, and hippocampal-dependent learning. Together, these results support measurements of circulating adropin as a conserved, translational biomarker of cognitive aging and a potential therapeutic target.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13639007/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148221303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Disentangling shifting demographic and treatment effects on years of life lost to cancer in Denmark. 在丹麦，人口结构的变化和治疗对癌症死亡年数的影响。

IF 13

npj aging Pub Date : 2026-06-09 DOI: 10.1038/s41514-026-00420-7

Ólafur Birgir Davíðsson, Emelie Hamotal Curovic-Rotbain, Ragnar Pétur Kristjánsson, Jojo Biel-Nielsen Dietz, Signe Holst Søegaard, Mikkel Werling, Fie Stegenborg Andersen, Susanne Dalton, Carsten Utoft Niemann, Mads Melbye, Søren Friis, Henrik Hjalgrim, Klaus Rostgaard

{"title":"Disentangling shifting demographic and treatment effects on years of life lost to cancer in Denmark.","authors":"Ólafur Birgir Davíðsson, Emelie Hamotal Curovic-Rotbain, Ragnar Pétur Kristjánsson, Jojo Biel-Nielsen Dietz, Signe Holst Søegaard, Mikkel Werling, Fie Stegenborg Andersen, Susanne Dalton, Carsten Utoft Niemann, Mads Melbye, Søren Friis, Henrik Hjalgrim, Klaus Rostgaard","doi":"10.1038/s41514-026-00420-7","DOIUrl":"10.1038/s41514-026-00420-7","url":null,"abstract":"Cancer is increasingly relevant to ageing societies, yet progress in cancer control is difficult to assess when population years of life lost (YLL) to cancer appear stable. Using Danish registers, we followed 4.26 million residents aged ≥50 years (1980-2019) and estimated YLL under observed and counterfactual scenarios, separating demography and incidence from post-diagnosis outcomes. From the 1980s to the 2010s, YLL per individual changed little (men 2.3 to 2.1; women 2.5 to 2.2), while YLL per patient fell markedly (men 8.5 to 5.2; women 9.3 to 5.8). With 2010s incidence and background mortality but 1980s management, YLL per individual would have been 4.2 (men) and 3.9 (women), showing that cancer control averted about half of the life-years otherwise lost. YLL reductions were largest for localized and regional disease (~60 and ~40%) and modest for distant stage (~15%), highlighting persistent losses in advanced cancer and growing survivorship-care needs.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13590599/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148213853","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Nasal administration of Protollin enhances monocyte phagocytosis and decreases CD8⁺ T cell cytotoxicity in subjects with early Alzheimer's disease: a Phase 1 clinical trial. 早期阿尔茨海默病患者鼻用Protollin增强单核细胞吞噬并降低CD8+ T细胞毒性：一项1期临床试验

IF 13

npj aging Pub Date : 2026-06-05 DOI: 10.1038/s41514-026-00397-3

Panayota Kolypetri, Patrick da Silva, Ronaldo S Francisco, Dan Frenkel, Rachael R Cecere, Pien C J Kiliaan, Federico Montini, Shrishti Saxena, William A Clementi, Xuejun Liu, Cheng Sun, Regan W Bergmark, Tarun Singhal, Taylor J Saraceno, Joseph Zimmermann, Seth A Gale, Dennis J Selkoe, Tanuja Chitnis, Howard L Weiner

{"title":"Nasal administration of Protollin enhances monocyte phagocytosis and decreases CD8+ T cell cytotoxicity in subjects with early Alzheimer's disease: a Phase 1 clinical trial.","authors":"Panayota Kolypetri, Patrick da Silva, Ronaldo S Francisco, Dan Frenkel, Rachael R Cecere, Pien C J Kiliaan, Federico Montini, Shrishti Saxena, William A Clementi, Xuejun Liu, Cheng Sun, Regan W Bergmark, Tarun Singhal, Taylor J Saraceno, Joseph Zimmermann, Seth A Gale, Dennis J Selkoe, Tanuja Chitnis, Howard L Weiner","doi":"10.1038/s41514-026-00397-3","DOIUrl":"10.1038/s41514-026-00397-3","url":null,"abstract":"Protollin, a nasal adjuvant, was evaluated in a randomized double-blind phase 1 study of 16 early Alzheimer's disease (AD) patients to determine safety and to assess its immunomodulatory effects. In a double-blind dose escalation study, subjects received nasal Protollin at doses of 0.1 mg, 0.5 mg, 1.0 mg, and 1.5 mg or placebo twice over a two-week period. Treatment was well-tolerated with minimal side effects. Transcriptomic and single-cell analyses demonstrated that prior to treatment, AD blood monocytes had downregulation of phagocytosis-related genes and an increased pro-inflammatory signature. These AD monocyte abnormalities were reversed by nasal Protollin beginning at a dose of 1.0 mg. Protollin induced a robust phagocytic gene signature, including upregulation of CD36, ITGAL, LYST, and FCGR1A. A similar phagocytic signature was observed in brain-infiltrating amyloid-clearing monocytes in an APP Tg mouse model treated with nasal Protollin. Protollin treatment decreased the expression of costimulatory molecules on monocytes and decreased CD8 + T cell activation and cytotoxicity. Our results provide the basis for a phase 2 study of nasal Protollin in subjects with AD in which nasal Protollin at a dose of 1.0 mg will be administered weekly over 6 months to modulate peripheral immunity and clear amyloid from the brain. ClinicalTrials.gov registration no NCT07187141.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":13.0,"publicationDate":"2026-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13558635/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177406","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Methylglyoxal engages aging-associated mechanisms to cause filtration impairment in nephrocytes. 甲基乙二醛参与衰老相关机制导致肾细胞滤过功能受损。

IF 6

npj aging Pub Date : 2026-06-04 DOI: 10.1038/s41514-026-00369-7

Lie Cheng, Wan-Ju Yeh, Fan-Chi Chang, Hong-Wen Tang, Chih-Chiang Chan, Shuei-Liong Lin, Shu-Yi Huang

{"title":"Methylglyoxal engages aging-associated mechanisms to cause filtration impairment in nephrocytes.","authors":"Lie Cheng, Wan-Ju Yeh, Fan-Chi Chang, Hong-Wen Tang, Chih-Chiang Chan, Shuei-Liong Lin, Shu-Yi Huang","doi":"10.1038/s41514-026-00369-7","DOIUrl":"https://doi.org/10.1038/s41514-026-00369-7","url":null,"abstract":"The decline of glomerular filtration is a hallmark of aging. Methylglyoxal (MG) is a uremic toxin known to induce aging-like changes; however, whether its mechanism of action is similar remains unclear. We compare the underlying mechanisms of MG and aging using Drosophila nephrocytes as a model. In addition to lower body weight, reduced locomotion, and shorter lifespans, MG caused filtration defects and induced cellular senescence in nephrocytes similar to the effects of aging, with a corresponding upregulation of the LXR/RXR signaling pathway. Mechanistically, we found that MG and aging both increased reactive oxygen species (ROS). Antioxidant treatments and inhibition of the LXR/RXR pathway both improved the filtration function. In addition, MG and aging both reduced the level of Jub, which is a protein essential for the integrity of the slit diaphragm structure. Overexpressing jub enhanced slit diaphragm structure and prevented MG-induced functional decline. Together, the findings reveal parallel features between MG and aging, and show that inhibiting LXR/RXR signaling, reducing ROS, or strengthening the slit diaphragm structure can preserve the filtration function of Drosophila nephrocytes.","PeriodicalId":94160,"journal":{"name":"npj aging","volume":" ","pages":""},"PeriodicalIF":6.0,"publicationDate":"2026-06-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148166303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0