Pub Date : 2026-01-09DOI: 10.1038/s43587-025-01055-1
Hannah Walters
{"title":"Evaluating music interventions to treat depression in people living with dementia","authors":"Hannah Walters","doi":"10.1038/s43587-025-01055-1","DOIUrl":"10.1038/s43587-025-01055-1","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"26-26"},"PeriodicalIF":19.4,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145947185","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}
Pub Date : 2026-01-09DOI: 10.1038/s43587-025-01051-5
Huaxiong Jiang
{"title":"Socioeconomic reforms are needed to address disparities for the aging rural-to-urban migrant workforce in China.","authors":"Huaxiong Jiang","doi":"10.1038/s43587-025-01051-5","DOIUrl":"https://doi.org/10.1038/s43587-025-01051-5","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":19.4,"publicationDate":"2026-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145946661","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}
Pub Date : 2026-01-05DOI: 10.1038/s43587-025-01060-4
Dominic Denk, Anurag Singh, Herbert G Kasler, Davide D'Amico, Julia Rey, Lucía Alcober-Boquet, Johanna M Gorol, Christoph Steup, Ritesh Tiwari, Ryan Kwok, Rafael J Argüello, Julie Faitg, Kathrin Sprinzl, Stefan Zeuzem, Valentina Nekljudova, Sibylle Loibl, Eric Verdin, Chris Rinsch, Florian R Greten
{"title":"Author Correction: Effect of the mitophagy inducer urolithin A on age-related immune decline: a randomized, placebo-controlled trial.","authors":"Dominic Denk, Anurag Singh, Herbert G Kasler, Davide D'Amico, Julia Rey, Lucía Alcober-Boquet, Johanna M Gorol, Christoph Steup, Ritesh Tiwari, Ryan Kwok, Rafael J Argüello, Julie Faitg, Kathrin Sprinzl, Stefan Zeuzem, Valentina Nekljudova, Sibylle Loibl, Eric Verdin, Chris Rinsch, Florian R Greten","doi":"10.1038/s43587-025-01060-4","DOIUrl":"https://doi.org/10.1038/s43587-025-01060-4","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":19.4,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907106","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}
Brain health is closely linked to bone homeostasis. Skeletal aging is characterized by inadequate bone formation and marrow adiposity, but whether the brain contributes to this imbalance remains unknown. This study shows that aged brain neurons, mainly those in the hippocampus and cerebral cortex, produce excess WD repeat and FYVE domain containing 1 (WDFY1) protein and transfer it to the bone via extracellular vesicles (EVs), leading to bone-fat imbalance and osteoporosis. Increasing brain Wdfy1 expression causes premature skeletal aging. Conversely, suppressing Wdfy1 in the whole brain, hippocampus or neurons, genetically deleting neuronal Wdfy1, and selectively inhibiting neuronal EV release all improve bone health. Mechanistically, WDFY1 binds to the retromer complex to promote the endosome-to-Golgi recycling of cathepsin D and peroxiredoxin 2, thus inhibiting osteogenesis and augmenting adipogenesis. This study identifies the role of aged brain neuronal EVs as an important messenger in triggering bone-fat imbalance by transferring WDFY1 to bone.
{"title":"Brain neuron-derived WDFY1 induces bone loss.","authors":"Chun-Yuan Chen, Zun Wang, Chun-Gu Hong, Yi-Juan Tan, Yan-Xin Duan, Yi Luo, Xin Wang, Hai-Jin Zeng, Jing-Yao Luo, Teng-Fei Wan, Hao Yin, Xi-Xi Liu, Hao Zhu, Yong Zhou, Zheng-Guang Wang, Ze-Hui He, Xin-Yue Hu, Guo-Wen Hu, Hai-Li Lang, Zhen-Xing Wang, Jia Cao, Shan-Shan Rao, Hui Xie","doi":"10.1038/s43587-025-01032-8","DOIUrl":"10.1038/s43587-025-01032-8","url":null,"abstract":"<p><p>Brain health is closely linked to bone homeostasis. Skeletal aging is characterized by inadequate bone formation and marrow adiposity, but whether the brain contributes to this imbalance remains unknown. This study shows that aged brain neurons, mainly those in the hippocampus and cerebral cortex, produce excess WD repeat and FYVE domain containing 1 (WDFY1) protein and transfer it to the bone via extracellular vesicles (EVs), leading to bone-fat imbalance and osteoporosis. Increasing brain Wdfy1 expression causes premature skeletal aging. Conversely, suppressing Wdfy1 in the whole brain, hippocampus or neurons, genetically deleting neuronal Wdfy1, and selectively inhibiting neuronal EV release all improve bone health. Mechanistically, WDFY1 binds to the retromer complex to promote the endosome-to-Golgi recycling of cathepsin D and peroxiredoxin 2, thus inhibiting osteogenesis and augmenting adipogenesis. This study identifies the role of aged brain neuronal EVs as an important messenger in triggering bone-fat imbalance by transferring WDFY1 to bone.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":19.4,"publicationDate":"2026-01-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145907081","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}
Pub Date : 2026-01-02DOI: 10.1038/s43587-025-01045-3
Marina Kolesnichenko
Aging erodes the regenerative capacity of the gut, which weakens barrier function and repair. Eskiocak, Gewolb, Shah, Rouse, Chowdhury and colleagues show that senescent epithelial cells accumulate and drive this decline. Selective elimination of cells that express the senescence-associated surface marker uPAR using senolytic chimeric antigen receptor T cells restores stem cell function and rejuvenates the aged mouse gut.
{"title":"Rejuvenating the aging gut by targeting senescence","authors":"Marina Kolesnichenko","doi":"10.1038/s43587-025-01045-3","DOIUrl":"10.1038/s43587-025-01045-3","url":null,"abstract":"Aging erodes the regenerative capacity of the gut, which weakens barrier function and repair. Eskiocak, Gewolb, Shah, Rouse, Chowdhury and colleagues show that senescent epithelial cells accumulate and drive this decline. Selective elimination of cells that express the senescence-associated surface marker uPAR using senolytic chimeric antigen receptor T cells restores stem cell function and rejuvenates the aged mouse gut.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"32-33"},"PeriodicalIF":19.4,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893120","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}
Pub Date : 2026-01-02DOI: 10.1038/s43587-025-01044-4
Chih-Ling Wang, Mary Mohrin
Two recent studies, from Shang et al. and Mejía-Ramírez et al., identify complementary mechanical mechanisms that regulate hematopoietic stem cell aging: external shear stress and internal nuclear envelope tension. These forces represent an evolutionary tradeoff between immediate immune defense and long-term stem cell maintenance.
{"title":"Squishing, squeezing and stretching age hematopoietic stem cells","authors":"Chih-Ling Wang, Mary Mohrin","doi":"10.1038/s43587-025-01044-4","DOIUrl":"10.1038/s43587-025-01044-4","url":null,"abstract":"Two recent studies, from Shang et al. and Mejía-Ramírez et al., identify complementary mechanical mechanisms that regulate hematopoietic stem cell aging: external shear stress and internal nuclear envelope tension. These forces represent an evolutionary tradeoff between immediate immune defense and long-term stem cell maintenance.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"29-31"},"PeriodicalIF":19.4,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893336","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}
Pub Date : 2026-01-02DOI: 10.1038/s43587-025-01039-1
Tongyao Shang, Li Zhao, Shibo Ying, Lida Su, Yue Yang, Jiadong Liu, Yingying Wang, Jipeng Xue, Cheng Cheng, Yixin Wu, Shiyao Chen, Hongmei Dong, Xuequn Chen, Hailin Ma, Qi Zhang, Tingbo Liang, Wei Yang, Ye Feng, Marong Fang, Xinjiang Lu
Hematopoietic stem cells (HSCs) reside in the bone marrow in a quiescent state, but can be mobilized into the blood in response to inflammation, cytokine stimulation, nervous activity or hypoxia. Chronic inflammation, a hallmark of aging, accelerates HSC aging by promoting myeloid-biased differentiation and reducing self-renewal capacity, yet the role of mechanical stimulation in regulating these processes remains poorly understood. Here, we found that PIEZO1 senses shear stress in blood flow to induce HSC proliferation and myelopoiesis. We show that shear stress induces PIEZO1-mediated ion currents and Ca2+ influx in both mouse and human HSCs, with downstream effects on proliferation and myeloid differentiation mediated via JAM3 and CAPN2 pathways. GsMTx4, a PIEZO1 antagonist, attenuated inflammation-induced aging in mice by inhibiting HSC activation. These findings link the mechanical sensor PIEZO1 to HSC proliferation and myeloid differentiation via multi-tiered signaling, highlighting its role in accelerating inflammation-induced aging. Shang, Zhao, Ying and colleagues report that the mechanosensor PIEZO1 senses blood shear stress in hematopoietic stem cells, driving proliferation and myeloid bias. This axis links mechanical force to inflammation-induced aging, and PIEZO1 emerges as a potential therapeutic target.
{"title":"Shear stress governs hematopoietic stem cell fate to promote inflammation-induced aging","authors":"Tongyao Shang, Li Zhao, Shibo Ying, Lida Su, Yue Yang, Jiadong Liu, Yingying Wang, Jipeng Xue, Cheng Cheng, Yixin Wu, Shiyao Chen, Hongmei Dong, Xuequn Chen, Hailin Ma, Qi Zhang, Tingbo Liang, Wei Yang, Ye Feng, Marong Fang, Xinjiang Lu","doi":"10.1038/s43587-025-01039-1","DOIUrl":"10.1038/s43587-025-01039-1","url":null,"abstract":"Hematopoietic stem cells (HSCs) reside in the bone marrow in a quiescent state, but can be mobilized into the blood in response to inflammation, cytokine stimulation, nervous activity or hypoxia. Chronic inflammation, a hallmark of aging, accelerates HSC aging by promoting myeloid-biased differentiation and reducing self-renewal capacity, yet the role of mechanical stimulation in regulating these processes remains poorly understood. Here, we found that PIEZO1 senses shear stress in blood flow to induce HSC proliferation and myelopoiesis. We show that shear stress induces PIEZO1-mediated ion currents and Ca2+ influx in both mouse and human HSCs, with downstream effects on proliferation and myeloid differentiation mediated via JAM3 and CAPN2 pathways. GsMTx4, a PIEZO1 antagonist, attenuated inflammation-induced aging in mice by inhibiting HSC activation. These findings link the mechanical sensor PIEZO1 to HSC proliferation and myeloid differentiation via multi-tiered signaling, highlighting its role in accelerating inflammation-induced aging. Shang, Zhao, Ying and colleagues report that the mechanosensor PIEZO1 senses blood shear stress in hematopoietic stem cells, driving proliferation and myeloid bias. This axis links mechanical force to inflammation-induced aging, and PIEZO1 emerges as a potential therapeutic target.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"88-107"},"PeriodicalIF":19.4,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893297","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}
Pub Date : 2026-01-02DOI: 10.1038/s43587-025-01047-1
We developed scMORE (single-cell multiomics regulon enrichment), a computational framework that integrates single-cell multiomics with genome-wide association study summary statistics to identify transcription factor–chromatin–gene regulatory networks (eRegulons) that underlie complex diseases. Applying scMORE to 31 traits (including Parkinson’s disease), we investigated immune- and aging-associated eRegulons, and revealed how genetic variants shape cell-type-specific regulatory programs.
{"title":"Linking single-cell multiomics with GWAS to reveal key regulators of disease risk","authors":"","doi":"10.1038/s43587-025-01047-1","DOIUrl":"10.1038/s43587-025-01047-1","url":null,"abstract":"We developed scMORE (single-cell multiomics regulon enrichment), a computational framework that integrates single-cell multiomics with genome-wide association study summary statistics to identify transcription factor–chromatin–gene regulatory networks (eRegulons) that underlie complex diseases. Applying scMORE to 31 traits (including Parkinson’s disease), we investigated immune- and aging-associated eRegulons, and revealed how genetic variants shape cell-type-specific regulatory programs.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"36-37"},"PeriodicalIF":19.4,"publicationDate":"2026-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145893034","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}
Lung aging is a multifactorial series of molecular alterations that leads to gradual deterioration of lung function and increased vulnerability to cancer. Tumor communicates with host organs partially through extracellular vesicles; however, the mechanistic drivers and consequences of lung aging in the context of cancer remain unclear. Here we identify cancer cell-secreted dimethylarginine dimethylaminohydrolase-1 (DDAH1) protein induces citrulline accumulation and promotes lung fibrosis and aging. Mechanistically, our single-cell sequencing and genetic knockout mice evidence that citrulline availability elevation inhibits peptidyl arginine deiminase 4-mediated transforming growth factor-β1 (TGF-β1) citrullination, thereby inducing the TGF-β1/Smad3 signaling pathway in lung fibroblasts. Notably, vacuolar protein sorting assists the packaging of DDAH1 into the late endosomes. The administration of DDAH1 inhibitor reduces fibrosis and alleviates lung aging. Conclusively, our findings reveal tumor-derived DDAH1 protein contributes to citrulline accumulation to promote lung aging, shedding light on the treatment and diagnosis of tumors by inhibiting senescent lung fibroblasts. Liu et al. show that tumor-secreted dimethylarginine dimethylaminohydrolase-1 protein induces citrulline accumulation and promotes lung fibrosis and aging, shedding light on the cancer treatment and diagnosis by inhibiting senescent lung fibroblasts.
{"title":"Cancer-cell-secreted DDAH1 induces TGF-β1/Smad3 signaling pathway to promote fibrosis and aging in lung","authors":"Liu Liu, Qianyue Wang, Meng Chen, Haifeng Zhou, Xu Li, Ziqi Yuan, Yong Hu, Chaoqun Wang, Xiaohui Zhang, Sheng Hu, Xiaoting Wu, Meixin Li, Juanjuan Li, Aijun Chen, Wei Yan","doi":"10.1038/s43587-025-01024-8","DOIUrl":"10.1038/s43587-025-01024-8","url":null,"abstract":"Lung aging is a multifactorial series of molecular alterations that leads to gradual deterioration of lung function and increased vulnerability to cancer. Tumor communicates with host organs partially through extracellular vesicles; however, the mechanistic drivers and consequences of lung aging in the context of cancer remain unclear. Here we identify cancer cell-secreted dimethylarginine dimethylaminohydrolase-1 (DDAH1) protein induces citrulline accumulation and promotes lung fibrosis and aging. Mechanistically, our single-cell sequencing and genetic knockout mice evidence that citrulline availability elevation inhibits peptidyl arginine deiminase 4-mediated transforming growth factor-β1 (TGF-β1) citrullination, thereby inducing the TGF-β1/Smad3 signaling pathway in lung fibroblasts. Notably, vacuolar protein sorting assists the packaging of DDAH1 into the late endosomes. The administration of DDAH1 inhibitor reduces fibrosis and alleviates lung aging. Conclusively, our findings reveal tumor-derived DDAH1 protein contributes to citrulline accumulation to promote lung aging, shedding light on the treatment and diagnosis of tumors by inhibiting senescent lung fibroblasts. Liu et al. show that tumor-secreted dimethylarginine dimethylaminohydrolase-1 protein induces citrulline accumulation and promotes lung fibrosis and aging, shedding light on the cancer treatment and diagnosis by inhibiting senescent lung fibroblasts.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"143-161"},"PeriodicalIF":19.4,"publicationDate":"2025-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829443","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}
Pub Date : 2025-12-19DOI: 10.1038/s43587-025-01026-6
Kai Zhuang, Liu Zi, Xiao Su, Chen Hu, Xinrui Li, Shuzhong Wang, Yujun Xia, Bo Wu, Yuemin Su, Shaokun Chen, Haojie Li, Siqi Wang, Mengdan Wang, Jieyin Li, Wenting Xie, Yanbing Chen, Lige Leng, Huifang Li, Li Zhong, Jiechao Zhou, Yan Liu, Qingsong Liu, Karl Herrup, Jie Zhang
Progressive neuronal loss and brain atrophy are principal determinants of cognitive decline in Alzheimer’s disease (AD), yet most mouse models fail to recapitulate these features. Here we identify cyclin-dependent kinase 3 (CDK3) as a key driver of neurodegeneration in AD. CDK3 is elevated in human AD brains and correlates with disease severity. As laboratory mice carry a nonfunctional Cdk3 mutation, we generated two models with restored CDK3 activity and then crossed to AD backgrounds. Both models exhibited substantial neuronal loss, hippocampal atrophy, and cognitive deficits. Single-nucleus RNA sequencing revealed neurons simultaneously activating cell cycle and cell death pathways, indicating cell cycle reentry-induced death. Proteomics implicated synaptic proteins as CDK3 substrates. Finally, we developed BMX330, an inhibitor of CDK3, which mitigated neuronal death and rescued cognitive decline in CDK3-restored AD mice. These findings position CDK3 as a therapeutic target and provide pathologically relevant AD models. Zhuang, Zi et al. identify cyclin-dependent kinase 3 (CDK3) as a driver of neuron loss in Alzheimer’s disease that is associated with brain atrophy and memory decline in mice. Inhibition of CDK3 (BMX330) is shown to limit neuronal loss and improve cognition.
{"title":"CDK3 induces neuronal death and brain atrophy in Alzheimer’s disease","authors":"Kai Zhuang, Liu Zi, Xiao Su, Chen Hu, Xinrui Li, Shuzhong Wang, Yujun Xia, Bo Wu, Yuemin Su, Shaokun Chen, Haojie Li, Siqi Wang, Mengdan Wang, Jieyin Li, Wenting Xie, Yanbing Chen, Lige Leng, Huifang Li, Li Zhong, Jiechao Zhou, Yan Liu, Qingsong Liu, Karl Herrup, Jie Zhang","doi":"10.1038/s43587-025-01026-6","DOIUrl":"10.1038/s43587-025-01026-6","url":null,"abstract":"Progressive neuronal loss and brain atrophy are principal determinants of cognitive decline in Alzheimer’s disease (AD), yet most mouse models fail to recapitulate these features. Here we identify cyclin-dependent kinase 3 (CDK3) as a key driver of neurodegeneration in AD. CDK3 is elevated in human AD brains and correlates with disease severity. As laboratory mice carry a nonfunctional Cdk3 mutation, we generated two models with restored CDK3 activity and then crossed to AD backgrounds. Both models exhibited substantial neuronal loss, hippocampal atrophy, and cognitive deficits. Single-nucleus RNA sequencing revealed neurons simultaneously activating cell cycle and cell death pathways, indicating cell cycle reentry-induced death. Proteomics implicated synaptic proteins as CDK3 substrates. Finally, we developed BMX330, an inhibitor of CDK3, which mitigated neuronal death and rescued cognitive decline in CDK3-restored AD mice. These findings position CDK3 as a therapeutic target and provide pathologically relevant AD models. Zhuang, Zi et al. identify cyclin-dependent kinase 3 (CDK3) as a driver of neuron loss in Alzheimer’s disease that is associated with brain atrophy and memory decline in mice. Inhibition of CDK3 (BMX330) is shown to limit neuronal loss and improve cognition.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"6 1","pages":"200-220"},"PeriodicalIF":19.4,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145795751","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}
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