Aging Cell最新文献

Featured Cover

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

引用次数: 0

Additional Cover

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

引用次数: 0

Telomeres in Space

IF 7.8 1区医学

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

Abraham Aviv, Simon Verhulst

引用次数: 0

Correction to “Antagonizing Peroxisome Proliferator-Activated Receptor γ Facilitates M1-To-M2 Shift of Microglia by Enhancing Autophagy via the LKB1-AMPK Signaling Pathway”

IF 7.8 1区医学

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

引用次数: 0

Exploring Lymph Node Stroma Ageing: Immune Implications and Future Directions

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

Featured Cover

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-13 DOI: 10.1111/acel.70017

Richie P. Goulding, Braeden T. Charlton, Ellen A. Breedveld, Matthijs van der Laan, Anne R. Strating, Wendy Noort, Aryna Kolodyazhna, Brent Appelman, Michèle van Vugt, Anita E. Grootemaat, Nicole N. van der Wel, Jos J. de Koning, Frank W. Bloemers, Rob C. I. Wüst

引用次数: 0

Correction to “Targeting miR-124/ Ferroportin Signaling Ameliorated Neuronal Cell Death Through Inhibiting Apoptosis and Ferroptosis in Aged Intracerebral Hemorrhage Murine Model”

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-13 DOI: 10.1111/acel.70006

引用次数: 0

Proteasome Augmentation Mitigates Age-Related Cognitive Decline in Mice

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-13 DOI: 10.1111/acel.14492

Danitra Parker, Kanisa Davidson, Pawel A. Osmulski, Maria Gaczynska, Andrew M. Pickering

{"title":"Proteasome Augmentation Mitigates Age-Related Cognitive Decline in Mice","authors":"Danitra Parker, Kanisa Davidson, Pawel A. Osmulski, Maria Gaczynska, Andrew M. Pickering","doi":"10.1111/acel.14492","DOIUrl":"10.1111/acel.14492","url":null,"abstract":"The aging brain experiences a significant decline in proteasome function. The proteasome is critical for many key neuronal functions including neuronal plasticity, and memory formation/retention. Treatment with proteasome inhibitors impairs these processes. Our study reveals a marked reduction in 20S and 26S proteasome activities in aged mice brains, including in the hippocampus, this is driven by reduced functionality of aged proteasome. The decline in proteasome activity is matched by a decline in 20S proteasome assembly. In contrast, 26S proteasome assembly was found to increase with age, though 26S proteasome activity was still found to decline. Our data suggests that age-related declines in proteasome activity is driven predominantly by reduced functionality of proteasome rather than altered composition. By overexpressing the proteasome subunit PSMB5 in the neurons of mice to increase the proteasome content and thus enhance its functionality, we slowed age-related declines in spatial learning and memory. We then showed acute treatment with a proteasome activator to rescue spatial learning and memory deficits in aged mice. These findings highlight the potential of proteasome augmentation as a therapeutic strategy to mitigate age-related cognitive declines.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14492","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143404975","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

RETRACTION: Bmi-1 Plays a Critical Role in Protection From Renal Tubulointerstitial Injury by Maintaining Redox Balance

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-12 DOI: 10.1111/acel.70012

{"title":"RETRACTION: Bmi-1 Plays a Critical Role in Protection From Renal Tubulointerstitial Injury by Maintaining Redox Balance","authors":"","doi":"10.1111/acel.70012","DOIUrl":"10.1111/acel.70012","url":null,"abstract":"RETRACTION: J. Jin, X. Lv, L. Chen, W. Zhang, J. Li, Q. Wang, R. Wang, X. Lu, and D. Miao, “Bmi-1 Plays a Critical Role in Protection From Renal Tubulointerstitial Injury by Maintaining Redox Balance,” Aging Cell 13, no. 5 (2014): 797–809, https://doi.org/10.1111/acel.12236.The above article, published online on 11 June 2014, in Wiley Online Library (wileyonlinelibrary.com), has been retracted by agreement between the journal Editor-in-Chief, Monty Montano; The Anatomical Society; and John Wiley & Sons Ltd. The retraction has been agreed upon following an investigation into concerns raised by a third party, which revealed image section duplications between this (Figure 3C, WT TNF-α panel) and another article that was subsequently published by an overlapping group of authors, where the image depicts different experimental details. The investigation discovered further image duplications, showing overlapping fields of view between Figure S3G Cortex and Medulla KO panels and between Figure S4C and S4D Medulla KO TNF-α and IL-6 panels. The explanation and the partial raw data shared by the authors was deemed insufficient to fully address these concerns. Thus, the editors have lost confidence in the presented data and decided to retract the article. The authors disagree with the retraction.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.70012","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143404976","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

Caloric Restriction and Telomere Preservation in TERT Knockout Adipocyte Progenitors Does Not Rescue Mice From Metabolic Dysfunction due to a TERT Function in Adipocyte Mitochondria

IF 7.8 1区医学

Aging Cell Pub Date : 2025-02-11 DOI: 10.1111/acel.14499

Zhanguo Gao, Yongmei Yu, Kristin Eckel-Mahan, Mikhail G. Kolonin

{"title":"Caloric Restriction and Telomere Preservation in TERT Knockout Adipocyte Progenitors Does Not Rescue Mice From Metabolic Dysfunction due to a TERT Function in Adipocyte Mitochondria","authors":"Zhanguo Gao, Yongmei Yu, Kristin Eckel-Mahan, Mikhail G. Kolonin","doi":"10.1111/acel.14499","DOIUrl":"10.1111/acel.14499","url":null,"abstract":"Inactivation of telomerase (TERT) in adipocyte progenitor cells (APC) expedites telomere attrition, and the onset of diabetes in mice fed high-fat diet (HFD), which promotes APC over-proliferation and replicative senescence. Here, we show that time-restricted feeding or caloric restriction in the postnatal development of mice subsequently subjected to HFD prevents telomere attrition but not glucose intolerance. This metabolic effect of dietary intervention was not observed for mice with TERT KO in endothelial or myeloid cells. To characterize the telomere-independent effects of TERT in the APC lineage, we analyzed mice with TERT knockout in mature adipocytes (AD-TERT-KO), which do not proliferate and avoid telomere attrition. Analysis of adipocytes from AD-TERT-KO mice indicated reliance on glycolysis and decreased mitochondrial oxidative metabolism. We show that AD-TERT-KO mice have reduced cold tolerance and metabolism abnormality indicating a defect in adaptive thermogenesis, characteristic of aging. Conversely, ectopic TERT expression in brown adipocytes-induced mitochondrial oxidation and thermogenic gene expression. We conclude that TERT plays an important non-canonical function in the mitochondria of adipocytes.","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14499","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143397710","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