Aging Cell最新文献

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IF 7.8 1区医学

Aging Cell Pub Date : 2025-04-10 DOI: 10.1111/acel.70073

Hyunho Lee, Matteo Massaro, Nourhan Abdelfattah, Gherardo Baudo, Haoran Liu, Kyuson Yun, Elvin Blanco

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Anatomical Society Research Studentships 2025/26 解剖学会研究奖学金2025/26

IF 7.8 1区医学

Aging Cell Pub Date : 2025-04-10 DOI: 10.1111/acel.70074

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IF 7.8 1区医学

Aging Cell Pub Date : 2025-04-10 DOI: 10.1111/acel.70072

Zhidi Lin, Guangyu Xu, Xiao Lu, Hongli Wang, Feizhou Lu, Xinlei Xia, Jian Song, Jianyuan Jiang, Xiaosheng Ma, Fei Zou

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IF 7.8 1区医学

Aging Cell Pub Date : 2025-03-11 DOI: 10.1111/acel.70045

Akash Kumar Singh, Ila Joshi, Neeharika M. N. Reddy, Sushmitha S. Purushotham, M. Eswaramoorthy, Madavan Vasudevan, Sourav Banerjee, James P. Clement, Tapas K. Kundu

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IF 7.8 1区医学

Aging Cell Pub Date : 2025-03-11 DOI: 10.1111/acel.70046

Akash Kumar Singh, Ila Joshi, Neeharika M. N. Reddy, Sushmitha S. Purushotham, M. Eswaramoorthy, Madavan Vasudevan, Sourav Banerjee, James P. Clement, Tapas K. Kundu, Tamunotonye Omoluabi, Zia Hasan, Jessie E. Piche, Abeni R. S. Flynn, Jules J. E. Doré, Susan G. Walling, Andrew C. W. Weeks, Touati Benoukraf, Qi Yuan

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Downregulation of NAD Kinase Expression in β-Cells Contributes to the Aging-Associated Decline in Glucose-Stimulated Insulin Secretion β-细胞中NAD激酶表达的下调有助于葡萄糖刺激胰岛素分泌的衰老相关下降。

IF 7.8 1区医学

Aging Cell Pub Date : 2025-03-05 DOI: 10.1111/acel.70037

Guan-Jie Li, Mei-Ling Cheng, Yu-Ting Lin, Yu-Hsuan Ho, Gigin Lin, Chih-Yung Chiu, Hung-Yao Ho

{"title":"Downregulation of NAD Kinase Expression in β-Cells Contributes to the Aging-Associated Decline in Glucose-Stimulated Insulin Secretion","authors":"Guan-Jie Li, Mei-Ling Cheng, Yu-Ting Lin, Yu-Hsuan Ho, Gigin Lin, Chih-Yung Chiu, Hung-Yao Ho","doi":"10.1111/acel.70037","DOIUrl":"10.1111/acel.70037","url":null,"abstract":"Nicotinamide adenine dinucleotide kinase (NADK) is essential to the generation of nicotinamide adenine dinucleotide phosphate (NADP(H)), an important metabolic coupling factor involved in glucose-stimulated insulin secretion. In the present study, we showed that the expression of Nadk and Nadk2 transcripts and NADP(H) content were lower in islets of 80-week-old (aged) mice than those of 8-week-old (young) mice. This was associated with diminished oral glucose tolerance of old mice and the glucose-stimulated insulin secretion (GSIS) response of islets. Knockdown (KD) of Nadk or Nadk2 gene expression in NIT-1 cells impaired glucose-stimulated insulin secretion. Metabolomic analysis revealed that Nadk KD specifically affected purine metabolism in glucose-stimulated cells. The levels of 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR) were higher in KD cells than in the non-targeting control (NTC) cells. Phosphorylation of AMP-activated protein kinase (AMPK) was elevated in glucose-treated KD cells compared to that of NTC cells. Increased AICAR level and AMPKα phosphorylation were observed in the glucose-stimulated islets of the aged mice. Genetic and pharmacological inhibition of AMPK promoted glucose-stimulated insulin release by KD cells and the aged mouse islets. It is likely that NADK is modulatory to AMPK activation in pancreatic β-cells and to their GSIS response. Enhanced AICAR formation in KD cells was accompanied by significantly increased conversion from inosine monophosphate (IMP) in a tetrahydrofolate (THF)-dependent manner. Folate supplementation augmented the GSIS response of KD cells and aged mouse islets. Taken together, these findings suggest that the aging-associated decline in NADK expression may underlie the reduced insulin secretory capacity of pancreatic β-cells.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-03-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70037","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Telomeres in Space 太空中的端粒。

IF 7.8 1区医学

Aging Cell Pub Date : 2025-03-01 DOI: 10.1111/acel.70030

Abraham Aviv, Simon Verhulst

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Correction to “Antagonizing Peroxisome Proliferator-Activated Receptor γ Facilitates M1-To-M2 Shift of Microglia by Enhancing Autophagy via the LKB1-AMPK Signaling Pathway” 更正“拮抗过氧化物酶体增殖物激活受体γ通过LKB1-AMPK信号通路增强自噬促进小胶质细胞m1 - m2转移”。

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-27 DOI: 10.1111/acel.70025

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Large-Scale Clustered Transcriptional Silencing Associated With Cellular Senescence 与细胞衰老相关的大规模集群转录沉默。

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-19 DOI: 10.1111/acel.70015

Aditi U. Gurkar, Satoshi Okawa, Christelle Guillermier, Kritika Chaddha, Matthew L. Steinhauser

{"title":"Large-Scale Clustered Transcriptional Silencing Associated With Cellular Senescence","authors":"Aditi U. Gurkar, Satoshi Okawa, Christelle Guillermier, Kritika Chaddha, Matthew L. Steinhauser","doi":"10.1111/acel.70015","DOIUrl":"10.1111/acel.70015","url":null,"abstract":"Senescence is a cell fate associated with age-related pathologies; however, senescence markers are not well-defined. Using single cell multi-isotope imaging mass spectrometry (MIMS), we identified hypercondensed, transcriptionally silent DNA globules in a senescence model induced by dysfunctional telomeres. This architectural phenomenon was associated with geographically clustered transcriptional repression across somatic chromosomes with over-representation of cell cycle genes. Senescence-stimuli was associated with a higher frequency of cells that exhibited geographically concentrated transcriptional repression relative to control cells. This phenomenon was also observed in multiple other senescence models, including replicative senescence and irradiation. We further identified an enrichment of common pathways in all models of senescence, suggesting a common cellular response to this silencing phenomenon. Such large-scale clustered silencing of chromosomal segments rather than individual genes may explain senescence heterogeneity and a putative trajectory toward deep, irreversible senescence.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70015","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143447760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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Exploring Lymph Node Stroma Ageing: Immune Implications and Future Directions 探索淋巴结基质老化：免疫意义和未来方向。

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-15 DOI: 10.1111/acel.70000

Yu Yang Ng, Andy Tay

{"title":"Exploring Lymph Node Stroma Ageing: Immune Implications and Future Directions","authors":"Yu Yang Ng, Andy Tay","doi":"10.1111/acel.70000","DOIUrl":"10.1111/acel.70000","url":null,"abstract":"Ageing is an inevitable biological process that impacts the immune system, leading to immunosenescence and inflammaging, which contribute to increased susceptibility to infections, autoimmune diseases and cancers in individuals over the age of 65. This review focuses on the ageing of lymph node stromal cells (LNSCs), which are crucial for maintaining lymph node (LN) structure and function. Age-related changes in LNs, such as fibrosis and lipomatosis, disrupt the LN architecture and reduce immune cell recruitment and function, impairing immune responses to infections and vaccinations. The review discusses the structural and functional decline of various LNSC subsets, including fibroblastic reticular cells (FRCs), lymphatic endothelial cells (LECs) and blood endothelial cells (BECs), highlighting their roles in immune cell activation and homeostasis. Potential strategies to restore aged LNSC function, such as enhancing LNSC activation during vaccination and using senotherapeutics, are explored. Outstanding questions regarding the mechanisms of LNSC ageing and how ageing of the LN stroma might impact autoimmune disorders are also addressed. This review aims to stimulate further research into the characterisation of aged LNSCs and the development of therapeutic interventions to improve immune function in the older adults.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-02-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70000","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143424460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0