Aging-Us最新文献_第3页

The cell rejuvenation atlas: leveraging network biology to identify master regulators of rejuvenation strategies. 细胞年轻化图谱：利用网络生物学识别年轻化策略的主调节因子。

IF 5.2 3区医学

Aging-Us Pub Date : 2024-09-09 DOI: 10.18632/aging.206105

Javier Arcos Hodar,Sascha Jung,Mohamed Soudy,Sybille Barvaux,Antonio Del Sol

{"title":"The cell rejuvenation atlas: leveraging network biology to identify master regulators of rejuvenation strategies.","authors":"Javier Arcos Hodar,Sascha Jung,Mohamed Soudy,Sybille Barvaux,Antonio Del Sol","doi":"10.18632/aging.206105","DOIUrl":"https://doi.org/10.18632/aging.206105","url":null,"abstract":"Current rejuvenation strategies, which range from calorie restriction to in vivo partial reprogramming, only improve a few specific cellular processes. In addition, the molecular mechanisms underlying these approaches are largely unknown, which hinders the design of more holistic cellular rejuvenation strategies. To address this issue, we developed SINGULAR (Single-cell RNA-seq Investigation of Rejuvenation Agents and Longevity), a cell rejuvenation atlas that provides a unified system biology analysis of diverse rejuvenation strategies across multiple organs at single-cell resolution. In particular, we leverage network biology approaches to characterize and compare the effects of each strategy at the level of intracellular signaling, cell-cell communication, and transcriptional regulation. As a result, we identified master regulators orchestrating the rejuvenation response and propose that targeting a combination of them leads to a more holistic improvement of age-dysregulated cellular processes. Thus, the interactive database accompanying SINGULAR is expected to facilitate the future design of synthetic rejuvenation interventions.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":5.2,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142217684","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Longitudinal activity monitoring and lifespan: quantifying the interface. 纵向活动监测与寿命：量化界面。

IF 5.2 3区医学

Aging-Us Pub Date : 2024-09-09 DOI: 10.18632/aging.206106

Su I Iao,Poorbita Kundu,Han Chen,James R Carey,Hans-Georg Müller

引用次数: 0

Decisive gene strategy on osteoarthritis: a comprehensive whole-literature based approach for conclusive gene targets. 骨关节炎的决定性基因策略：基于全文献的决定性基因靶点综合方法。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-06 DOI: 10.18632/aging.206094

Yi-Chou Chen, Yu-Chiao Wang, Meng-Chang Lee, Yu-Hsuan Chen, Wen Su, Pi-Shao Ko, Cheng-Jung Chen, Sui-Lung Su

{"title":"Decisive gene strategy on osteoarthritis: a comprehensive whole-literature based approach for conclusive gene targets.","authors":"Yi-Chou Chen, Yu-Chiao Wang, Meng-Chang Lee, Yu-Hsuan Chen, Wen Su, Pi-Shao Ko, Cheng-Jung Chen, Sui-Lung Su","doi":"10.18632/aging.206094","DOIUrl":"10.18632/aging.206094","url":null,"abstract":"Background: Previous meta-analyses only examined the association between single or several gene polymorphisms and osteoarthritis (OA), whereas no studies have concluded that there are existing all gene loci that associate with OA.Objective: To assess whether a definite conclusion of the association between the gene loci and OA can be drawn.Methods: Decisive gene strategy (DGS), a literature-based approach, was used to search PubMed, Embase, and Cochrane databases for all meta-analyses that associated gene polymorphisms and OA. Trial Sequential Analysis (TSA) examined the sufficiency of the cumulative sample size. Finally, we assessed the importance of gene loci in OA based on whether there were enough sample sizes and the heterogeneity of the literatures with I2 value.Results: After excluding 179 irrelevant publications, 80 meta-analysis papers were recruited. Among Caucasians, SMAD3 rs12901499 (OR = 1.20, 95% CI: 1.12-1.29) was a risk factor with validation of sufficient sample sizes through TSA model. Among Asians, there were 3 gene loci risk factors with validation of sufficient sample sizes through TSA model: ESR1 rs2228480, SMAD3 rs12901499, and MMP-1 rs1799750 (OR = 1.35, 95% CI: 1.08-1.69; OR = 1.34, 95% CI: 1.07-1.69; OR = 1.43, 95% CI: 1.18-1.74, respectively). Besides, 3 gene loci, DVWA rs7639618, GDF5 rs143383, and VDR rs7975232 (OR = 0.78, 95% CI: 0.67-0.90; OR = 0.74, 95% CI: 0.67-0.81; OR = 0.56, 95% CI: 0.35-0.90, respectively) were identified as protective factors through TSA model.Conclusions: We used DGS to identify conclusive gene loci associated with OA. These findings provide implications of precision medicine in OA and may potentially advance genetic therapy.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424587/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142156756","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

MTA2 knockdown suppresses human osteosarcoma metastasis by inhibiting uPA expression. 通过抑制uPA的表达敲除MTA2抑制人骨肉瘤的转移

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-06 DOI: 10.18632/aging.206070

Chun Tseng, Chien-Min Chen, Yi-Hsien Hsieh, Chia-Yu Lin, Jian-Wen Chen, Pang-Hsuan Hsiao, Yi-Chin Fong, Pei-Han Wang, Pei-Ni Chen, Renn-Chia Lin

{"title":"MTA2 knockdown suppresses human osteosarcoma metastasis by inhibiting uPA expression.","authors":"Chun Tseng, Chien-Min Chen, Yi-Hsien Hsieh, Chia-Yu Lin, Jian-Wen Chen, Pang-Hsuan Hsiao, Yi-Chin Fong, Pei-Han Wang, Pei-Ni Chen, Renn-Chia Lin","doi":"10.18632/aging.206070","DOIUrl":"10.18632/aging.206070","url":null,"abstract":"The relationship between metastasis-associated protein 2 (MTA2) overexpression and tumor growth and metastasis has been extensively studied in a variety of tumor cells but not in human osteosarcoma cells. This study aims to elucidate the clinical significance, underlying molecular mechanisms, and biological functions of MTA2 in human osteosarcoma in vitro and in vivo. Our results show that MTA2 was elevated in osteosarcoma cell lines and osteosarcoma tissues and was associated with tumor stage and overall survival of osteosarcoma patients. Knockdown of MTA2 inhibited osteosarcoma cell migration and invasion by reducing the expression of urokinase-type plasminogen activator (uPA). Bioinformatic analysis demonstrated that high levels of uPA in human osteosarcoma tissues correlated positively with MTA2 expression. Furthermore, treatment with recombinant human uPA (Rh-uPA) caused significant restoration of OS cell migration and invasion in MTA2 knockdown osteosarcoma cells. We found that ERK1/2 depletion increased the expression of uPA, facilitating osteosarcoma cell migration and invasion. Finally, MTA2 depletion significantly reduced tumor metastasis and the formation of lung nodules in vivo. Overall, our study suggests that MTA2 knockdown suppresses osteosarcoma cell metastasis by decreasing uPA expression via ERK signaling. This finding provides new insight into potential treatment strategies against osteosarcoma metastasis by targeting MTA2.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424574/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142156757","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 joint protective function of live- and dead-Lactobacillus plantarum GKD7 on anterior cruciate ligament transection induces osteoarthritis. 植物乳杆菌 GKD7 的活菌和死菌对前十字韧带横断引起的骨关节炎的关节保护功能

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-05 DOI: 10.18632/aging.206101

Yen-You Lin, Chih-Ying Wu, You-Shan Tsai, Chin-Chu Chen, Tzu-Ching Chang, Li-Chai Chen, Hsien-Te Chen, Chin-Jung Hsu, Chih-Hsin Tang

{"title":"The joint protective function of live- and dead-Lactobacillus plantarum GKD7 on anterior cruciate ligament transection induces osteoarthritis.","authors":"Yen-You Lin, Chih-Ying Wu, You-Shan Tsai, Chin-Chu Chen, Tzu-Ching Chang, Li-Chai Chen, Hsien-Te Chen, Chin-Jung Hsu, Chih-Hsin Tang","doi":"10.18632/aging.206101","DOIUrl":"https://doi.org/10.18632/aging.206101","url":null,"abstract":"Osteoarthritis (OA) is a chronic inflammatory disease accompanied by joint pain, bone degradation, and synovial inflammation. Tumor necrosis factor (TNF)-α and interleukin (IL)-1β play key roles in chronic inflammation, and matrix metalloproteinase (MMP)3 is the first enzyme released by chondrocytes and synovial cells that promotes MMPs' degrading cartilage matrix (including collage II and aggrecan) function. Using an anterior cruciate ligament transection (ACLT) rat model, Lactobacillus plantarum GKD7 has shown anti-inflammatory and analgesic properties. The present investigation examined the chondroprotective effects of several dosages and formulas of GKD7 on rats in an ACLT-induced OA model. The findings indicate that oral treatment with both live-GKD7 (GKD7-L) and dead-GKD7 (GKD7-D), along with celecoxib (positive control), all reduce post-ACLT pain and inflammation in OA joints. Subsequently, the immunohistochemical staining results demonstrate that following GKD7-L and GKD7-D treatment, there was a reversal of the degradation of collagen II and aggrecan, as well as a decrease in the expression of IL-1β and TNF-α on the synovial tissue and MMP3 on the cartilage. Accordingly, our findings imply that the treatment of both GKD7-L and GKD7-D has chondroprotective and analgesic effects on the OA rat model, and that celecoxib and GKD7-L at dosages (100 mg/kg) have comparable therapeutic benefits. As a result, we propose that both GKD7-L and GKD7-D are helpful supplements for OA management.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Poor sleep quality, dementia status and their association with all-cause mortality among older US adults. 美国老年人睡眠质量差、痴呆状态及其与全因死亡率的关系。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-04 DOI: 10.18632/aging.206102

May A Beydoun, Rio Tate, Michael F Georgescu, Alyssa A Gamaldo, Christian A Maino Vieytes, Hind A Beydoun, Nicole Noren Hooten, Michele K Evans, Alan B Zonderman

{"title":"Poor sleep quality, dementia status and their association with all-cause mortality among older US adults.","authors":"May A Beydoun, Rio Tate, Michael F Georgescu, Alyssa A Gamaldo, Christian A Maino Vieytes, Hind A Beydoun, Nicole Noren Hooten, Michele K Evans, Alan B Zonderman","doi":"10.18632/aging.206102","DOIUrl":"10.18632/aging.206102","url":null,"abstract":"Background: Evidence points to associations between sleep quality, dementia, and mortality. We examined whether poor sleep quality mediated or moderated the association between dementia and mortality risk among older US adults and vice versa, and whether these associations differed by sex and by race.Methods: The study investigated bi-directional associations between sleep quality, dementia and mortality in older US adults using data from the Health and Retirement Study (N = 6,991, mean age = 78.1y, follow-up: 2006-2020, number of deaths = 4,938). It tested interactions and mediating effects, using Cox proportional hazards models and four-way decomposition models.Results: Poor sleep quality was associated with increased mortality risk, particularly among male and White older adults. However, the association was reversed in the fully adjusted model, with a 7% decrease in risk per tertile. Probable dementia was associated with a two-fold increase in mortality risk, with a stronger association found among White adults. The association was markedly attenuated in the fully adjusted models. Sleep quality-stratified models showed a stronger positive association between dementia and mortality among individuals with better sleep quality. Both mediation and interaction were involved in explaining the total effects under study, though statistically significant total effects were mainly composed of controlled direct effects.Conclusions: Poor sleep quality is directly related to mortality risk before lifestyle and health-related factors are adjusted. Dementia is linked to mortality risk, especially in individuals with better sleep quality, males, and White older adults. Future research should explore the underlying mechanisms.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424588/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141821","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

Wenshenqianlie capsule improves benign prostatic hyperplasia via its anti-inflammatory and antioxidant effects. 温神前列胶囊通过抗炎和抗氧化作用改善良性前列腺增生。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-04 DOI: 10.18632/aging.206103

Rui Liu, Zhen Sun, Shimiao Wang, Xin Liu, Yuhong Man, Meiwan Chen, Qian Liu, Chunyue Wang

{"title":"Wenshenqianlie capsule improves benign prostatic hyperplasia via its anti-inflammatory and antioxidant effects.","authors":"Rui Liu, Zhen Sun, Shimiao Wang, Xin Liu, Yuhong Man, Meiwan Chen, Qian Liu, Chunyue Wang","doi":"10.18632/aging.206103","DOIUrl":"https://doi.org/10.18632/aging.206103","url":null,"abstract":"Anti-inflammatory and antioxidant effects play crucial roles in the recovery of benign prostatic hyperplasia (BPH). Wenshenqianlie (WSQL) capsule, a typical traditional Chinese medicine formulation combining 14 Chinese herbs, has been reported to exert tonic effects on the kidneys and improve clinical symptoms of BPH. However, its potential antioxidative and anti-inflammatory properties and effects on the improvement of hormone levels have not been reported in depth. In this study, mice were subcutaneously injected with TP (5 mg/kg·d-1) to induce BPH. Forty-eight adult BALB/c male mice were randomly allocated to six groups based on the type of drug administered by gavage: control, BPH, BPH+WSQL (40 and 80 mg/kg·d-1), BPH+finasteride (1 mg/kg·d-1), and WSQL-only treated (80 mg/kg·d-1). We investigated the anti-inflammatory and antioxidant effect and mechanism of WSQL on BPH via histopathological examination, immunohistochemistry, enzyme-linked immunosorbent assay, and western blotting combined with in vivo serum metabolomics, gut microbiomics analysis. WSQL alleviated prostate hyperplasia and reduced prostate-specific antigen, dihydrotestosterone, testosterone, and inflammation levels. Gut microbiomics and serum non-targeted metabolomics determined that the protective effect of WSQL against BPH may be related to the improvement of inflammation and testosterone-related gut microbiota and serum metabolites. Further studies showed that WSQL ameliorated nuclear factor-kappa B, its downstream inflammatory factors, and nuclear factor E2-related factor 2 pathway.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142141820","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Melatonin downregulates angiogenesis and lymphangiogenesis by regulating tumor-associated macrophages via NLRP3 inflammasomes in lung adenocarcinoma. 褪黑素通过NLRP3炎症小体调节肺腺癌中的肿瘤相关巨噬细胞，从而下调血管生成和淋巴管生成。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-09-03 DOI: 10.18632/aging.206057

Zhewei Zhao, Dongjie Ma, Yingzhi Qin, Yuan Xu, Shanqing Li, Hongsheng Liu

{"title":"Melatonin downregulates angiogenesis and lymphangiogenesis by regulating tumor-associated macrophages via NLRP3 inflammasomes in lung adenocarcinoma.","authors":"Zhewei Zhao, Dongjie Ma, Yingzhi Qin, Yuan Xu, Shanqing Li, Hongsheng Liu","doi":"10.18632/aging.206057","DOIUrl":"10.18632/aging.206057","url":null,"abstract":"Tumor-associated macrophages (TAMs), present within the tumor microenvironment (TME), strictly modulate tumor angiogenesis and lymphangiogenesis. Nevertheless, the associated signaling networks and candidate drug targets for these events remains to be elucidated. Given its antioxidative activities, we speculated that melatonin may reduce pyroptosis, and thereby modulate both angiogenesis and lymphangiogenesis. We revealed that a co-culture of A549 cells and THP-1 macrophages strongly enhanced expressions of the NLRP3 inflammasome axis members, and augmented angiogenesis and lymphangiogenesis. Next, we overexpressed NLRP3 in the A549 cells, and demonstrated that excess NLRP3 expression substantially upregulated VEGF and CXCL cytokine expressions, and enhanced lymphatic endothelial cells (LECs) tube formation. In contrast, NLRP3 inhibition produced the opposite effect. In addition, relative to controls, melatonin administration strongly inhibited the NLRP3 inflammasome axis, as well as angiogenesis and lymphangiogenesis in the co-culture system. Subsequent animal experiments using a Lewis Lung Carcinoma (LLC) subcutaneous tumor model in mice corroborate these findings. Melatonin treatment and NLRP3 knockdown significantly inhibit tumor growth and downregulate NLRP3 and IL-1β expression in tumor tissues. Furthermore, melatonin downregulates the expression of angiogenic and lymphangiogenic markers in tumor tissues. Taken together, the evidence suggested that a THP-1 macrophage and A549 cell co-culture stimulates angiogenesis and lymphangiogenesis via the NLRP3 axis. Melatonin protected against the TAMs- and NLRP3 axis-associated promotion of the aforementioned events in vitro and in vivo. Hence, melatonin is a promising candidate for managing for tumor-related angiogenesis and lymphangiogenesis in lung adenocarcinoma.","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-09-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11424589/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142127474","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

Retraction of: MicroRNA-346 facilitates cell growth and metastasis, and suppresses cell apoptosis in human non-small cell lung cancer by regulation of XPC/ERK/Snail/E-cadherin pathway. 撤回：MicroRNA-346通过调控XPC/ERK/Snail/E-cadherin通路促进人非小细胞肺癌的细胞生长和转移并抑制细胞凋亡

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-31 DOI: 10.18632/aging.205987

Cheng-Cao Sun, Shu-Jun Li, Zhan-Peng Yuan, De-Jia Li

引用次数: 0

Correction for: Araloside C attenuates atherosclerosis by modulating macrophage polarization via Sirt1-mediated autophagy. 更正为阿罗苷 C 通过 Sirt1 介导的自噬调节巨噬细胞极化，从而减轻动脉粥样硬化。

IF 3.9 3区医学

Aging-Us Pub Date : 2024-08-31 DOI: 10.18632/aging.206100

Yun Luo, Shan Lu, Ye Gao, Ke Yang, Daoshun Wu, Xudong Xu, Guibo Sun, Xiaobo Sun

引用次数: 0