Aging-Us最新文献_第5页

Correction for: Maternal high sugar and fat diet benefits offspring brain function via targeting on the gut-brain axis. 更正：母亲的高糖和高脂肪饮食通过瞄准肠-脑轴而有益于后代的脑功能。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-31 DOI: 10.18632/aging.206229

Dongdong Wang, Haiting Zhang, Miao Zeng, Xiaocui Tang, Xiangxiang Zhu, Yinrui Guo, Longkai Qi, Yizhen Xie, Mei Zhang, Diling Chen

引用次数: 0

Retraction of: Apigenin inhibits growth and migration of fibroblasts by suppressing FAK signaling. 收缩：芹菜素通过抑制FAK信号抑制成纤维细胞的生长和迁移。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-31 DOI: 10.18632/aging.206230

Hongyi Wang, Bingyu Guo, Shixiu Lin, Peng Chang, Kai Tao

引用次数: 0

Mesenchymal stem cell-specific Sirt1 overexpression prevents sarcopenia induced by 1,25-dihydroxyvitamin D deficiency. 间充质干细胞特异性Sirt1过表达可预防1,25-二羟基维生素D缺乏引起的肌肉减少症。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-31 DOI: 10.18632/aging.206232

Haiyun Chen, Biqi Ren, Jing Wang, Xingchen Liu, Xiangjiao Yi, David Goltzman, Dengshun Miao

{"title":"Mesenchymal stem cell-specific Sirt1 overexpression prevents sarcopenia induced by 1,25-dihydroxyvitamin D deficiency.","authors":"Haiyun Chen, Biqi Ren, Jing Wang, Xingchen Liu, Xiangjiao Yi, David Goltzman, Dengshun Miao","doi":"10.18632/aging.206232","DOIUrl":"10.18632/aging.206232","url":null,"abstract":"Sarcopenia, characterized by an age-related decline in skeletal muscle mass and function, is closely linked to vitamin D deficiency. This study examines the role of Sirtuin 1 (Sirt1) and its regulation by vitamin D in preventing sarcopenia. Utilizing wild-type, 1α-hydroxylase knockout (1α(OH)ase-/-), and Sirt1 transgenic (Sirt1Tg) 1α(OH)ase-/- mice, we investigated muscle Sirt1 levels, muscle mass, fiber type, and senescence markers. Our results demonstrated that 1,25-Dihydroxyvitamin D (1,25(OH)2D3) upregulated Sirt1 and myogenic factor MyoD1 expression in C2C12 myoblasts via VDR-mediated transcription. Sirt1 overexpression in mesenchymal stem cells (MSCs) significantly mitigated muscle mass reduction, improved fiber cross-sectional area, and increased type II fiber numbers in 1α(OH)ase-/- mice. Mechanistically, 1,25(OH)2D3 promoted muscle cell health by enhancing Sirt1 expression, which in turn reduced muscle cell senescence and the senescence-associated secretory phenotype (SASP) through decreased levels of acetylated nuclear p53 and p65, maintaining their cytoplasmic localization. Additionally, Sirt1 overexpression accelerated muscle regeneration post-injury by increasing embryonic myosin heavy chain expression and cell proliferation. These findings underscore the therapeutic potential of targeting vitamin D and Sirt1 pathways to prevent sarcopenia, suggesting that supplementation with active vitamin D and consequent Sirt1 activation could be effective strategies for managing age-related muscle wasting.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"1026-1042"},"PeriodicalIF":3.9,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074815/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143765961","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer's disease. 正常与a β相关胆碱酯酶的差异抗衰老抑制：衰老和阿尔茨海默病的意义

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-29 DOI: 10.18632/aging.206227

Sultan Darvesh, Meghan K Cash, Katrina Forrestall, Hillary Maillet, Dane Sands

{"title":"Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer's disease.","authors":"Sultan Darvesh, Meghan K Cash, Katrina Forrestall, Hillary Maillet, Dane Sands","doi":"10.18632/aging.206227","DOIUrl":"10.18632/aging.206227","url":null,"abstract":"Cellular senescence is a hallmark of aging and the age-related condition, Alzheimer's disease (AD). How senescence contributes to cholinergic and neuropathologic changes in AD remains uncertain. Furthermore, little is known about the relationship between senescence and cholinesterases (ChEs). Acetylcholinesterase (AChE) and butyrylcholinesterase (BChE) are important in neurotransmission, cell cycle regulation, and AD amyloid-β (Aβ) pathology. Senolytic agents have shown therapeutic promise in AD models. Therefore, we evaluated in vitro and in silico activity of senolytics, dasatinib (1), nintedanib (2), fisetin (3), quercetin (4), GW2580 (5), and nootropic, meclofenoxate hydrochloride (6), toward AChE and BChE. As ChEs associated with AD pathology have altered biochemical properties, we also evaluated agents 1-6 in AD brain tissues. Enzyme kinetics showed agents 1, 3, 4, and 6 inhibited both ChEs, while 2 and 5 inhibited only AChE. Histochemistry showed inhibition of Aβ plaque-associated ChEs (1 and 2: both ChEs; 5: BChE; 6: AChE), but not normal neural-associated ChEs. Modeling studies showed 1-6 interacted with the same five binding locations of both ChEs, some of which may be allosteric sites. These agents may exert their beneficial effects, in part, by inhibiting ChEs associated with AD pathology and provide new avenues for development of next-generation inhibitors targeting pathology-associated ChEs.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"822-850"},"PeriodicalIF":3.9,"publicationDate":"2025-03-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984419/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143755999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

The rodent aging interventions database (RAID): a data visualization tool for all studies reporting rodent lifespan extension. 啮齿动物衰老干预数据库（RAID）：一个数据可视化工具，用于所有报告啮齿动物寿命延长的研究。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-27 DOI: 10.18632/aging.206228

Maximus V Peto, Anthony J Floyd, Ben Zealley, Aubrey D N J de Grey

{"title":"The rodent aging interventions database (RAID): a data visualization tool for all studies reporting rodent lifespan extension.","authors":"Maximus V Peto, Anthony J Floyd, Ben Zealley, Aubrey D N J de Grey","doi":"10.18632/aging.206228","DOIUrl":"10.18632/aging.206228","url":null,"abstract":"Numerous studies have investigated the effects of various interventions on the lifespans of mice and rats. The design of future rodent lifespan extension experiments might consider experimental parameters used in earlier investigations, but finding and reviewing all previous experiments requires a substantial resource investment. Additionally, when studied collectively, the results of previous investigations might suggest fundamental mechanisms causing age-related degeneration. Here, we report our efforts to find and aggregate data from all research reports of lifespan extension in mice or rats, which we call the \"Rodent Aging Interventions Database\" (RAID). We identified studies for inclusion using complex PubMed queries and by nomination from our colleagues in the field. The relevant data from each study was manually extracted and recorded in a table. A publicly available, web-based software tool was then created to enable users to visualize and filter this data in a convenient manner. Our current dataset, covering publications up to October 2022, includes 121 unique studies reporting on 212 distinct intervention protocols that extended lifespan in mice or rats. We intend to periodically update our dataset as new rodent lifespan studies are reported. RAID is publicly available at https://levf.org/raid.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"851-862"},"PeriodicalIF":3.9,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984422/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143744507","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Decreased surface receptors, function, and suboptimal osteoclasts-induced cell expansion in natural killer (NK) cells of elderly subjects. 老年人自然杀伤（NK）细胞中表面受体、功能和破骨细胞诱导细胞扩增的减少。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-26 DOI: 10.18632/aging.206226

Kawaljit Kaur, Anahid Jewett

{"title":"Decreased surface receptors, function, and suboptimal osteoclasts-induced cell expansion in natural killer (NK) cells of elderly subjects.","authors":"Kawaljit Kaur, Anahid Jewett","doi":"10.18632/aging.206226","DOIUrl":"10.18632/aging.206226","url":null,"abstract":"Natural killer (NK) cells are known for their cytotoxic and cytokine secretion capabilities. The balance of activating and inhibitory receptors on their surface regulates NK cell function and survival. However, it is not fully understood how aging may modulate the levels of NK cell surface receptors ultimately affecting their interaction with other immune cells, especially with those known to activate and expand NK cells. Here, we report decreased levels of NK cells' surface receptors, cytotoxic function, and cytokine secretion in aged donors (75-85 years) as compared to younger donors (21-25 years). We used our previously established methodology to expand and supercharge NK cells from young and older individuals using osteoclasts (OCs) and probiotic bacteria. Significantly lower levels of NK cell expansion and functional activation were seen in NK cells from 75-85-year-old donors when compared to younger donors' NK cells. Surface receptors of OCs were also found to be decreased in 75-85-year-old donors compared to younger donors. In addition, OCs from 75-85-year-old donors induced lower levels of cell expansion and functional activation of NK cells when compared to OCs from younger donors. These findings illustrate defects in both peripheral blood-derived primary NK cells and OCs in older individuals; however, suppression appears to be more in NK cells when compared to OCs.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"798-821"},"PeriodicalIF":3.9,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984426/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143732871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Parallel patterns of age-related working memory impairment in marmosets and macaques. 狨猴和猕猴年龄相关工作记忆损伤的平行模式。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-24 DOI: 10.18632/aging.206225

Casey R Vanderlip, Megan L Jutras, Payton A Asch, Stephanie Y Zhu, Monica N Lerma, Elizabeth A Buffalo, Courtney Glavis-Bloom

{"title":"Parallel patterns of age-related working memory impairment in marmosets and macaques.","authors":"Casey R Vanderlip, Megan L Jutras, Payton A Asch, Stephanie Y Zhu, Monica N Lerma, Elizabeth A Buffalo, Courtney Glavis-Bloom","doi":"10.18632/aging.206225","DOIUrl":"10.18632/aging.206225","url":null,"abstract":"As humans age, some experience cognitive impairment while others do not. When impairment does occur, it is not expressed uniformly across cognitive domains and varies in severity across individuals. Translationally relevant model systems are critical for understanding the neurobiological drivers of this variability, which is essential to uncovering the mechanisms underlying the brain's susceptibility to the effects of aging. As such, non-human primates (NHPs) are particularly important due to shared behavioral, neuroanatomical, and age-related neuropathological features with humans. For many decades, macaque monkeys have served as the primary NHP model for studying the neurobiology of cognitive aging. More recently, the common marmoset has emerged as an advantageous model for this work due to its short lifespan that facilitates longitudinal studies. Despite their growing popularity as a model, whether marmosets exhibit patterns of age-related cognitive impairment comparable to those observed in macaques and humans remains unexplored. To address this major limitation for the development and evaluation of the marmoset as a model of cognitive aging, we directly compared working memory ability as a function of age in macaques and marmosets on the identical task. We also implemented varying delays to further tax working memory capacity. Our findings demonstrate that marmosets and macaques exhibit remarkably similar age-related working memory deficits, with macaques performing better than marmosets on longer delays. These results highlight the similarities and differences between the two most commonly used NHP models and support the value of the marmoset as a model for cognitive aging research within the neuroscience community.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"778-797"},"PeriodicalIF":3.9,"publicationDate":"2025-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984434/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143712251","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP). 抑制金属蛋白酶ADAM19作为一种新的形态学策略，通过调节衰老相关分泌表型（SASP）来改善肠道通透性和衰老标志物

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-20 DOI: 10.18632/aging.206224

Sudipta Bar, Tyler A U Hilsabeck, Blaine Pattavina, José Alberto López-Domínguez, Nathan Basisty, Joanna Bons, Mark Watson, Birgit Schilling, Judith Campisi, Pankaj Kapahi, Amit Sharma

{"title":"Inhibition of the metalloprotease ADAM19 as a novel senomorphic strategy to ameliorate gut permeability and senescence markers by modulating senescence-associated secretory phenotype (SASP).","authors":"Sudipta Bar, Tyler A U Hilsabeck, Blaine Pattavina, José Alberto López-Domínguez, Nathan Basisty, Joanna Bons, Mark Watson, Birgit Schilling, Judith Campisi, Pankaj Kapahi, Amit Sharma","doi":"10.18632/aging.206224","DOIUrl":"10.18632/aging.206224","url":null,"abstract":"Accumulation of DNA damage can accelerate aging through cellular senescence. Previously, we established a Drosophila model to investigate the effects of radiation-induced DNA damage on the intestine. In this model, we examined irradiation-responsive senescence in the fly intestine. Through an unbiased genome-wide association study (GWAS) utilizing 156 strains from the Drosophila Genetic Reference Panel (DGRP), we identified meltrin (the drosophila orthologue of mammalian ADAM19) as a potential modulator of the senescence-associated secretory phenotype (SASP). Knockdown of meltrin resulted in reduced gut permeability, DNA damage, and expression of the senescence marker β-galactosidase (SA-β-gal) in the fly gut following irradiation. Additionally, inhibition of ADAM19 in mice using batimastat-94 reduced gut permeability and inflammation in the gut. Our findings extend to human primary fibroblasts, where ADAM19 knockdown or pharmacological inhibition decreased expression of specific SASP factors and SA-β-gal. Furthermore, proteomics analysis of the secretory factor of senescent cells revealed a significant decrease in SASP factors associated with the ADAM19 cleavage site. These data suggest that ADAM19 inhibition could represent a novel senomorphic strategy.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"757-777"},"PeriodicalIF":3.9,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984429/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143674959","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance. 人工饲养的橄榄狒狒（Papio anubis）的表观遗传和加速年龄，以及与行走速度和精细运动表现的关系。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-18 DOI: 10.18632/aging.206223

Sarah J Neal, Shannon Whitney, Soojin V Yi, Joe H Simmons

{"title":"Epigenetic and accelerated age in captive olive baboons (Papio anubis), and relationships with walking speed and fine motor performance.","authors":"Sarah J Neal, Shannon Whitney, Soojin V Yi, Joe H Simmons","doi":"10.18632/aging.206223","DOIUrl":"10.18632/aging.206223","url":null,"abstract":"Epigenetic age, estimated by DNA methylation across the genome, reflects biological age. Accelerated age (i.e., an older methylation age than expected given chronological age) is an accepted aging biomarker in humans, showing robust associations with deleterious health outcomes, longevity, and mortality. However, data regarding age acceleration in nonhuman primates (NHPs), and relationships between NHP epigenetic age and behavioral indicators of aging, such as walking speed and fine motor performance, are sparse. We measured DNA methylation of 140 captive olive baboons (Papio anubis) (84% female, 3-20 years-old), estimated their epigenetic ages, and classified them as showing age acceleration or deceleration. We found that epigenetic age was strongly correlated with chronological age, and that approximately 27% of the sample showed age acceleration and 28% showed age deceleration. We subsequently examined relationships between epigenetic and accelerated age and walking speed (N=129) and fine motor performance (N=39). Older animals showed slower speeds and poorer motor performance. However, the difference between the epigenetic age and chronological age, referred to as delta age, was not a consistent predictor of walking speed or fine motor performance. These data highlight the need for further examination of age acceleration across NHP species, and the ways that age acceleration may (not) be related to indicators of aging in NHP models.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"740-756"},"PeriodicalIF":3.9,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984432/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143658775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness. 成骨细胞线粒体氧化应激或自噬减少不足以模拟衰老对骨机械反应性的有害影响。

IF 3.9 3区医学

Aging-Us Pub Date : 2025-03-18 DOI: 10.18632/aging.206213

Ana Resende-Coelho, Md Mohsin Ali, Alicen James, Aaron Warren, Landon Gatrell, Ilham Kadhim, Qiang Fu, Jinhu Xiong, Melda Onal, Maria Almeida

{"title":"Mitochondrial oxidative stress or decreased autophagy in osteoblast lineage cells is not sufficient to mimic the deleterious effects of aging on bone mechanoresponsiveness.","authors":"Ana Resende-Coelho, Md Mohsin Ali, Alicen James, Aaron Warren, Landon Gatrell, Ilham Kadhim, Qiang Fu, Jinhu Xiong, Melda Onal, Maria Almeida","doi":"10.18632/aging.206213","DOIUrl":"10.18632/aging.206213","url":null,"abstract":"Exercise-induced mechanical load stimulates bone cells, including osteocytes, to promote bone formation. The bone response to loading is less effective with aging, but the cellular and molecular mechanisms responsible for the impaired mechanoresponsiveness remain unclear. Excessive mitochondrial reactive oxygen species (mtROS) and deficient autophagy are common aging mechanisms implicated in decreased bone formation in old mice. Here, we confirmed that the osteogenic effects of tibia compressive loading are lower in old versus young female mice. We also examined whether an increase in mtROS or decreased autophagy in osteoblast-lineage cells of adult female mice could mimic the deleterious effects of aging. To this end, we loaded mice lacking the antioxidant enzyme superoxide dismutase 2 (Sod2) or autophagy-related 7 (Atg7) in cells targeted by Osterix1 (Osx1)-Cre. Osteocytes in Atg7ΔOsx1 exhibited altered morphology and decreased osteocyte dendrite projections. Two weeks of loading increased cortical bone mass and bone formation rate at both periosteal and endosteal surfaces of Osx1-Cre control mice. Nonetheless, in both Atg7ΔOsx1 and Sod2ΔOsx1 mice the response to loading was identical to that observed in control mice, indicating that compromised Atg7-dependent autophagy or excessive mtROS are not sufficient to impair the bone response to tibial compressive loading. Thus, alternative mechanisms of aging might be responsible for the decreased response of the aged skeleton to mechanical stimuli. These findings also suggest that an intact osteocyte dendrite network is not required for the osteogenic response in this model of bone loading.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"610-629"},"PeriodicalIF":3.9,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143658793","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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