Aging Cell最新文献

{"title":"Associations of clinical parameter-based accelerated aging, genetic predisposition with risk of chronic kidney disease and associated life expectancy: A prospective cohort study","authors":"Gang Zheng,&nbsp;Qing Chang,&nbsp;Yixiao Zhang,&nbsp;Yashu Liu,&nbsp;Chao Ji,&nbsp;Honghao Yang,&nbsp;Liangkai Chen,&nbsp;Yang Xia,&nbsp;Yuhong Zhao","doi":"10.1111/acel.14453","DOIUrl":"10.1111/acel.14453","url":null,"abstract":"<p>Little evidence exists regarding the associations between clinical parameter-based biological aging and the incidence and outcome of chronic kidney disease (CKD). Thus, we aimed to assess the associations between biological aging, genetic risk, and the risk of CKD, as well as investigate the impact of accelerated biological aging on life expectancy. 281,363 participants free of kidney diseases from the UK Biobank were included in this prospective study. Biological age was measured from clinical traits using the KDM-BA and PhenoAge algorithms, and the discrepancies from chronological age were defined as biological age accelerations. A polygenic score was calculated to indicate the genetic predisposition of the estimated glomerular filtration rate (eGFR). A cause-specific competing risk model was used to estimate hazard ratios (HRs) and the corresponding confidence intervals (CIs) of incident CKD. We found that individuals with more pronounced accelerations in biological age exhibited an elevated risk of developing CKD (HR_{Quartile 4 vs. Quartile 1}, 1.90; 95% CI, 1.77–2.05 for KDM-BA acceleration and HR_{Quartile 4 vs. Quartile 1}, 2.79; 95% CI, 2.58–3.01 for PhenoAge acceleration), with nonlinear relationships. Notably, there were positive additive interactions between biological aging and genetic risk on CKD risk. Among the CKD population, accelerated biological aging was associated with a further decline in life expectancy. Advanced biological aging may potentially increase the vulnerability to developing CKD in individuals aged midlife and beyond, particularly among those with high genetic risk for abnormal kidney function, and could reduce the life expectancy of CKD patients.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14453","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142880758","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}

{"title":"A subset of human dermal fibroblasts overexpressing Cockayne syndrome group B protein resist UVB radiation-mediated premature senescence","authors":"Asimina Fotopoulou,&nbsp;Maria T. Angelopoulou,&nbsp;Harris Pratsinis,&nbsp;Eleni Mavrogonatou,&nbsp;Dimitris Kletsas","doi":"10.1111/acel.14422","DOIUrl":"10.1111/acel.14422","url":null,"abstract":"<p>Ultraviolet B (UVB) radiation is a major contributor to skin photoaging. Although mainly absorbed by the epidermis, UVB photons managing to penetrate the upper dermis affect human dermal fibroblasts (HDFs), leading, among others, to the accumulation of senescent cells. In vitro studies have shown that repeated exposures to subcytotoxic UVB radiation doses provoke HDFs' premature senescence shortly after the end of the treatment period. Here, we found that repetitive exposures to non-cytotoxic UVB radiation doses after several days lead to mixed cultures, containing both senescent cells and fibroblasts resisting senescence. “Resistant” fibroblasts were more resilient to a novel intense UVB radiation stimulus. RNA-seq analysis revealed that ERCC6, encoding Cockayne syndrome group B (CSB) protein, is up-regulated in resistant HDFs compared to young and senescent cells. CSB was found to be a key molecule conferring protection toward UVB-induced cytotoxicity and senescence, as siRNA-mediated CSB loss-of-expression rendered HDFs significantly more susceptible to a high UVB radiation dose, while cells from a CSB-deficient patient were found to be more sensitive to UVB-mediated toxicity, as well as senescence. UVB-resistant HDFs remained normal (able to undergo replicative senescence) and non-tumorigenic. Even though they formed a distinct population in-between young and senescent cells, resistant HDFs retained numerous tissue-impairing characteristics of the senescence-associated secretory phenotype, including increased matrix metalloprotease activity and promotion of epidermoid tumor xenografts in immunodeficient mice. Collectively, here we describe a novel subpopulation of HDFs showing increased resistance to UVB-mediated premature senescence while retaining undesirable traits that may negatively affect skin homeostasis.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14422","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142851654","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}

{"title":"Multi-omic analysis of biological aging biomarkers in long-term calorie restriction and endurance exercise practitioners: A cross-sectional study","authors":"Giovanni Fiorito,&nbsp;Valeria Tosti,&nbsp;Silvia Polidoro,&nbsp;Beatrice Bertozzi,&nbsp;Nicola Veronese,&nbsp;Edda Cava,&nbsp;Francesco Spelta,&nbsp;Laura Piccio,&nbsp;Dayna S. Early,&nbsp;Daniel Raftery,&nbsp;Paolo Vineis,&nbsp;Luigi Fontana","doi":"10.1111/acel.14442","DOIUrl":"10.1111/acel.14442","url":null,"abstract":"<p>Calorie restriction (CR) and physical exercise (EX) are well-established interventions known to extend health span and lifespan in animal models. However, their impact on human biological aging remains unclear. With recent advances in omics technologies and biological age (BioAge) metrics, it is now possible to assess the impact of these lifestyle interventions without the need for long-term follow-up. This study compared BioAge biomarkers in 41 middle-aged and older adult long-term CR practitioners, 41 age- and sex-matched endurance athletes (EX), and 35 sedentary controls consuming Western diets (WD), through PhenoAge: a composite score derived from nine blood-biomarkers. Additionally, a subset of participants (12 CR, 11 EX, and 12 WD) underwent multi-omic profiling, including DNA methylation and RNAseq of colon mucosa, blood metabolomics, and stool metagenomics. A group of six young WD subjects (yWD) served as a reference for BioAge calculation using Mahalanobis distance across six omic layers. The results demonstrated consistently lower BioAge biomarkers in both CR and EX groups compared to WD controls across all layers. CR participants exhibited lower BioAge in gut microbiome and blood-derived omics, while EX participants had lower BioAge in colon mucosa-derived epigenetic and transcriptomic markers, suggesting potential tissue-specific effects. Multi-omic pathway enrichment analyses suggested both shared and intervention-specific mechanisms, including oxidative stress and basal transcription as common pathways, with ether lipid metabolism uniquely enriched in CR. Despite limitations due to sample size, these findings contribute to the broader understanding of the potential anti-aging effects of CR and EX, offering promising directions for further research.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14442","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142845554","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}

{"title":"Age-Dependent Bi-Phasic Dynamics of Ly49+CD8+ Regulatory T Cell Population","authors":"Saranya Srinivasan,&nbsp;Shruti Mishra,&nbsp;Kenneth Ka-Ho Fan,&nbsp;Liwen Wang,&nbsp;John Im,&nbsp;Courtney Segura,&nbsp;Neelam Mukherjee,&nbsp;Gang Huang,&nbsp;Manjeet Rao,&nbsp;Chaoyu Ma,&nbsp;Nu Zhang","doi":"10.1111/acel.14461","DOIUrl":"10.1111/acel.14461","url":null,"abstract":"<p>Aging is tightly associated with reduced immune protection but increased risk of autoimmunity and inflammatory conditions. Regulatory T cells are one of the key cells to maintaining immune homeostasis. The age-dependent changes in CD4⁺Foxp3⁺ regulatory T cells (Tregs) have been well documented. However, the nonredundant Foxp3⁻CD8⁺ Tregs were never examined in the context of aging. This study first established clear distinctions between phenotypically overlapping CD8⁺ Tregs and virtual memory T cells. Then, we elucidated the dynamics of CD8⁺ Tregs across the lifespan in mice and further extended our investigation to human peripheral blood mononuclear cells (PBMCs). In mice, we discovered a bi-phasic dynamic shift in the frequency of CD8⁺CD44^hiCD122^hiLy49⁺ Tregs, with a steady increase in young adults and a notable peak in middle age followed by a decline in older mice. Transcriptomic analysis revealed that mouse CD8⁺ Tregs upregulated a selected set of natural killer (NK) cell-associated genes, including NKG2D, with age. Importantly, NKG2D might negatively regulate CD8⁺ Tregs. Additionally, by analyzing a scRNA-seq dataset of human PBMC, we found a distinct CD8⁺ Treg-like subset (Cluster 10) with comparable age-dependent frequency changes and gene expression, suggesting a conserved aging pattern in CD8⁺ Treg across mice and humans. In summary, our findings highlight the importance of CD8⁺ Tregs in immune regulation and aging.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14461","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142851670","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}

{"title":"Role of PI3K/AKT/MAOA in glucocorticoid-induced oxidative stress and associated premature senescence of the trabecular meshwork","authors":"Pengyu Zhang,&nbsp;Nan Zhang,&nbsp;Yixin Hu,&nbsp;Xizhi Deng,&nbsp;Min Zhu,&nbsp;Cheng Lai,&nbsp;Wen Zeng,&nbsp;Min Ke","doi":"10.1111/acel.14452","DOIUrl":"10.1111/acel.14452","url":null,"abstract":"<p>The oxidative stress-induced premature senescence of trabecular meshwork (TM) represents a pivotal risk factor for the development of glucocorticoid-induced glaucoma (GIG). This study aimed to elucidate the pathogenesis of TM senescence in GIG. MethodsIntraocular pressure (IOP), transmission electron microscopy and senescence-associated protein expression in TM were evaluated in GIG mice. Protein expression of phosphoinositide-3-kinase regulatory subunit 1 (PIK3R1) and monoamine oxidase A (MAOA), phosphorylation of AKT were quantified. ROS and mitochondrial superoxide levels were measured to evaluate cellular oxidative stress. Cell cycle analysis, β-galactosidase staining, senescence-associated protein expression were employed to assess the aging status of primary human trabecular meshwork cells (pHTMs). ResultsmRNA-seq and KEGG analysis indicating PI3K/AKT pathway as a key regulator in TM of GIG. PI3K inhibitor significantly prevented IOP elevation and abnormal mitochondrial morphology of TM in the GIG mouse model. PI3K inhibitor or selective silencing of <i>PIK3R1</i> alleviated dexamethasone (DEX)-induced oxidative stress, also mitochondrial dysfunction, inhibiting MAOA expression in pHTMs. The same phenomenon was observed in the GIG models with inhibition of MAOA. Further KEGG analysis indicates that cellular senescence is the key factor in the pathogenesis of GIG. TM senescence was observed in both GIG mouse and cell models. Inhibition of the PI3K/AKT/MAOA pathway significantly alleviated DEX-induced premature cellular senescence of TM in GIG models. Glucocorticoids activated the PI3K/AKT/MAOA pathway, leading to mitochondrial dysfunction, oxidative stress, and premature aging in TM, elevating IOP. This mechanism could be associated with the onset and progression of GIG, providing a potential approach for its treatment.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14452","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833194","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}

{"title":"Increased mitochondrial mutation heteroplasmy induces aging phenotypes in pluripotent stem cells and their differentiated progeny","authors":"Amy R. Vandiver,&nbsp;Alejandro Torres Jr,&nbsp;Amberly Sanden,&nbsp;Thang L. Nguyen,&nbsp;Jasmine Gasilla,&nbsp;Mary T. Doan,&nbsp;Vahan Martirosian,&nbsp;Austin Hoang,&nbsp;Jonathan Wanagat,&nbsp;Michael A. Teitell","doi":"10.1111/acel.14402","DOIUrl":"10.1111/acel.14402","url":null,"abstract":"<p>The mitochondrial genome (mtDNA) is an important source of inherited extranuclear variation. Clonal increases in mtDNA mutation heteroplasmy have been implicated in aging and disease, although the impact of this shift on cell function is challenging to assess. Reprogramming to pluripotency affects mtDNA mutation heteroplasmy. We reprogrammed three human fibroblast lines with known heteroplasmy for deleterious mtDNA point or deletion mutations. Quantification of mutation heteroplasmy in the resulting 76 induced pluripotent stem cell (iPSC) clones yielded a bimodal distribution, creating three sets of clones with high levels or absent mutation heteroplasmy with matched nuclear genomes. iPSC clones with elevated deletion mutation heteroplasmy show altered growth dynamics, which persist in iPSC-derived progenitor cells. We identify transcriptomic and metabolic shifts consistent with increased investment in neutral lipid synthesis as well as increased epigenetic age in high mtDNA deletion mutation iPSC, consistent with changes occurring in cellular aging. Together, these data demonstrate that high mtDNA mutation heteroplasmy induces changes occurring in cellular aging.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 3","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14402","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142833193","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}

{"title":"Age-associated accumulation of RAB9 disrupts oocyte meiosis","authors":"Min Gao,&nbsp;Fang Wang,&nbsp;Tengteng Xu,&nbsp;Yanling Qiu,&nbsp;Tianqi Cao,&nbsp;Simiao Liu,&nbsp;Wenlian Wu,&nbsp;Yitong Zhou,&nbsp;Haiying Liu,&nbsp;Fenghua Liu,&nbsp;Junjiu Huang","doi":"10.1111/acel.14449","DOIUrl":"10.1111/acel.14449","url":null,"abstract":"<p>The critical role of some RAB family members in oocyte meiosis has been extensively studied, but their role in oocyte aging remains poorly understood. Here, we report that the vesicle trafficking regulator, RAB9 GTPase, is essential for oocyte meiosis and aging in humans and mice. RAB9 was mainly located at the meiotic spindle periphery and cortex during oocyte meiosis. In humans and mice, we found that the RAB9 protein level were significantly increased in old oocytes. Age-related accumulation of RAB9 inhibits first polar body extrusion and reduces the developmental potential of oocytes. Further studies showed that increased Rab9 disrupts spindle formation and chromosome alignment. In addition, Rab9 overexpression disrupts the actin cap formation and reduces the cortical actin levels. Mechanically, Rab9-OE increases ROS levels, decreases mitochondrial membrane potential, ATP content and the mtDNA/nDNA ratio. Further studies showed that Rab9-OE activates the PINK1-PARKIN mitophagy pathway. Importantly, we found that reducing RAB9 protein expression in old oocytes could partially improve the rate of old oocyte maturation, ameliorate the accumulation of age-related ROS levels and spindle abnormalities, and partially rescue ATP levels, mtDNA/nDNA ratio, and PINK1 and PARKIN expression. In conclusion, our results suggest that RAB9 is required to maintain the balance between mitochondrial function and meiosis, and that reducing RAB9 expression is a potential strategy to ameliorate age-related deterioration of oocyte quality.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14449","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142826799","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}

{"title":"Organellar quality control crosstalk in aging-related disease: Innovation to pave the way","authors":"Yu Li,&nbsp;Jinxin Qi,&nbsp;Linhong Guo,&nbsp;Xian Jiang,&nbsp;Gu He","doi":"10.1111/acel.14447","DOIUrl":"10.1111/acel.14447","url":null,"abstract":"<p>Organellar homeostasis and crosstalks within a cell have emerged as essential regulatory and determining factors for the survival and functions of cells. In response to various stimuli, cells can activate the organellar quality control systems (QCS) to maintain homeostasis. Numerous studies have demonstrated that dysfunction of QCS can lead to various aging-related diseases such as neurodegenerative, pulmonary, cardiometabolic diseases and cancers. However, the interplay between QCS and their potential role in these diseases are poorly understood. In this review, we present an overview of the current findings of QCS and their crosstalk, encompassing mitochondria, endoplasmic reticulum, Golgi apparatus, ribosomes, peroxisomes, lipid droplets, and lysosomes as well as the aberrant interplays among these organelles that contributes to the onset and progression of aging-related disorders. Furthermore, potential therapeutic approaches based on these quality control interactions are discussed. Our perspectives can enhance insights into the regulatory networks underlying QCS and the pathology of aging and aging-related diseases, which may pave the way for the development of novel therapeutic targets.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11709098/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142816701","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}

{"title":"Association of metabolomic aging acceleration and body mass index phenotypes with mortality and obesity-related morbidities","authors":"Xiaomin Zeng,&nbsp;Ruiye Chen,&nbsp;Danli Shi,&nbsp;Xiayin Zhang,&nbsp;Ting Su,&nbsp;Yaxin Wang,&nbsp;Yijun Hu,&nbsp;Mingguang He,&nbsp;Honghua Yu,&nbsp;Xianwen Shang","doi":"10.1111/acel.14435","DOIUrl":"10.1111/acel.14435","url":null,"abstract":"<p>This study aims to investigate the association between metabolomic aging acceleration and body mass index (BMI) phenotypes with mortality and obesity-related morbidities (ORMs). 85,458 participants were included from the UK Biobank. Metabolomic age was determined using 168 metabolites. The Chronological Age-Adjusted Gap was used to define metabolomically younger (MY) or older (MO) status. BMI categories were defined as normal weight, overweight, and obese. Participants were categorized into MY normal weight (MY-NW, reference), MY overweight (MY-OW), MY obesity (MY-OB), MO normal weight (MO-NW), MO overweight (MO-OW), and MO obesity (MO-OB). Mortality and 43 ORMs were identified through death registries and hospitalization records. Compared with MY-NW phenotype, MO-OB phenotype yielded increased risk of mortality and 32 ORMs, followed by MO-OW with mortality and 27 ORMs, MY-OB with mortality and 26 ORMs, MY-OW with 21 ORMs, and MO-NW with mortality and 14 ORMs. Consistently, MO-OB phenotype showed the highest risk of developing obesity-related multimorbidities, followed by MY-OB phenotype, MO-OW phenotype, MY-OW phenotype, and MO-NW phenotype. Additive interactions were found between metabolomic aging acceleration and obesity on CVD-specific mortality and 10 ORMs. Additionally, individuals with metabolomic aging acceleration had higher mortality and cardiovascular risk, even within the same BMI category. These findings suggest that metabolomic aging acceleration could help stratify mortality and ORMs risk across different BMI categories. Weight management should also be extended to individuals with overweight or obesity even in the absence of accelerated metabolomic aging, as they face increased healthy risk compared with MY-NW individuals. Additionally, delaying metabolic aging acceleration is needed for all metabolomically older groups, including those with normal weight</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 4","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14435","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142811497","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}

{"title":"Additional Cover","authors":"Ken-ichi Takayama,&nbsp;Takashi Suzuki,&nbsp;Kaoru Sato,&nbsp;Yuko Saito,&nbsp;Satoshi Inoue","doi":"10.1111/acel.14456","DOIUrl":"https://doi.org/10.1111/acel.14456","url":null,"abstract":"<p>Cover legend: The cover image is based on the article <i>Cooperative nuclear action of RNA-binding proteins PSF and G3BP2 to sustain neuronal cell viability is decreased in aging and\u0000dementia</i> by Satoshi Inoue et al., https://doi.org/10.1111/acel.14316.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 12","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14456","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142868351","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}