Aging and Disease最新文献_第9页

Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis. 代谢重构与翻译后修饰：揭开骨质疏松症骨转换机制的神秘面纱。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-26 DOI: 10.14336/AD.2025.0123

Yuanyuan Li, Qilin Li, Kehan Zhang, Yaxin Wu, Gaoshaer Nuerlan, Xiangyao Wang, Yuxiao Zhang, Ahsawle Ozathaley, Jing Mao, Yan Liu, Shiqiang Gong

{"title":"Metabolic Rewiring and Post-Translational Modifications: Unlocking the Mechanisms of Bone Turnover in Osteoporosis.","authors":"Yuanyuan Li, Qilin Li, Kehan Zhang, Yaxin Wu, Gaoshaer Nuerlan, Xiangyao Wang, Yuxiao Zhang, Ahsawle Ozathaley, Jing Mao, Yan Liu, Shiqiang Gong","doi":"10.14336/AD.2025.0123","DOIUrl":"https://doi.org/10.14336/AD.2025.0123","url":null,"abstract":"Osteoporosis is a metabolic disease characterized by low bone density resulting from abnormal bone metabolism, caused by impaired osteogenesis and/or excessive bone resorption. The coordinated differentiation of osteoblasts (originating from mesenchymal stem cells) and osteoclasts (derived from hematopoietic progenitor cells) is necessary for maintaining normal bone remodeling and homeostasis. Metabolites have been confirmed to regulate cellular behavior through post-translational modifications (PTMs), including acetylation, lactylation, and succinylation. During osteoblast and osteoclast differentiation, progenitor cells undergo metabolic rewiring to meet the energy demands of these biological processes. Consequently, local metabolite profiles and intermediate metabolic products dynamically change during bone remodeling, influencing cell differentiation via PTMs. Given the regulatory role of PTMs in bone metabolism, this review systematically examines PTMs involved in osteoblast and osteoclast differentiation and explores potential avenues for addressing osteoporosis.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735556","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Exploring the Mechanisms of Testicular Aging: Advances in Biomarker Research. 睾丸衰老机制的探索：生物标志物研究进展。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-26 DOI: 10.14336/AD.2025.0070

Wenkang Chen, Hede Zou, Haoran Xu, Rui Cao, Yapeng Zhang, Yongjie Ma, Wei Lin, Hekun Zhang, Jiayou Zhao

{"title":"Exploring the Mechanisms of Testicular Aging: Advances in Biomarker Research.","authors":"Wenkang Chen, Hede Zou, Haoran Xu, Rui Cao, Yapeng Zhang, Yongjie Ma, Wei Lin, Hekun Zhang, Jiayou Zhao","doi":"10.14336/AD.2025.0070","DOIUrl":"https://doi.org/10.14336/AD.2025.0070","url":null,"abstract":"Aging biomarkers quantify aging progression and provide actionable targets for therapeutic interventions to mitigate age-related decline. This review synthesizes emerging evidence on testicular aging biomarkers, focusing on cellular senescence (Leydig, Sertoli, and endothelial cells), protein homeostasis disruption, mitochondrial dysfunction, germ stem cell depletion, sperm telomere length, epigenetic alterations, oxidative stress, inflammation, and gut microbiota dysbiosis. We propose that testicular aging serves as a critical nexus linking reproductive decline with systemic aging processes, with its pathological progression being quantifiable through specific biomarkers including the Leydig, Sertoli, and endothelial cells, INSL3, ribosomal protein RPL39L, sperm telomere length, relative telomere length mitochondrial translocator protein, and sialic acid. By bridging systemic aging paradigms with testis-specific mechanisms, we emphasize the urgency to identify organ-selective biomarkers for targeted interventions, advancing strategies to preserve male fertility and address population aging challenges.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Inflammatory Bridges: Interconnections Between Alzheimer's Disease and Bone Health. 炎症桥梁：阿尔茨海默病与骨骼健康之间的相互联系。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-25 DOI: 10.14336/AD.2025.10319

Hengrui Li, Wendi Wang, Liping Zhang, Tianwei Wang, Jian Liu, Jingguo Wu, Qingbin Ni, Baoliang Sun, Jingyi Sun

{"title":"Inflammatory Bridges: Interconnections Between Alzheimer's Disease and Bone Health.","authors":"Hengrui Li, Wendi Wang, Liping Zhang, Tianwei Wang, Jian Liu, Jingguo Wu, Qingbin Ni, Baoliang Sun, Jingyi Sun","doi":"10.14336/AD.2025.10319","DOIUrl":"https://doi.org/10.14336/AD.2025.10319","url":null,"abstract":"Alzheimer's disease is a neurodegenerative disorder that predominantly affects the elderly and is characterized by complex pathogenesis. Within the unified framework of the ANT, the introduction of B (the disruption of the blood-brain barrier) facilitates communication between the brain and the periphery through the blood-brain barrier. In this context, inflammatory factors act as a bridge, and the neuroinflammation hypothesis is gaining increasing acceptance. This hypothesis involves the abnormal activation of microglia, the release of inflammatory mediators, and damage to astrocytes, which leads to blood-brain barrier impairment and subsequently triggers systemic inflammation. Bone health is associated with conditions such as osteoporosis, osteoarthritis, rheumatoid arthritis, and periodontitis. This hypothesis establishes a link between Alzheimer's disease and bone health. The present article aims to construct an inflammatory bridge between brain and bone health by summarizing the shared mechanisms between the two, specifically focusing on age-related NLRP3-induced pyroptosis, advanced glycation end products, oxidative stress, macrophage autophagy and lysosomal function, and calcium ion dysregulation. Additionally, it reviews the latest therapeutic approaches to explore potential clinical treatments related to the connection between Alzheimer's disease and bone health through these shared mechanisms.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Interconnected Pathways of Alzheimer's Disease and Osteoporosis: A Review of Genetic, Hormonal, and Environmental Influences. 阿尔茨海默病和骨质疏松症的相互联系途径：遗传、激素和环境影响的综述。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-25 DOI: 10.14336/AD.2024.1438

Yu-Xin Li, Kun Liu, Qin Zeng, Wei-Hong Zeng, Jia-Li Li, Qian-Qian Zhang, Xuan Lu, Hong-Wen Deng, Li-Jun Tan

{"title":"Interconnected Pathways of Alzheimer's Disease and Osteoporosis: A Review of Genetic, Hormonal, and Environmental Influences.","authors":"Yu-Xin Li, Kun Liu, Qin Zeng, Wei-Hong Zeng, Jia-Li Li, Qian-Qian Zhang, Xuan Lu, Hong-Wen Deng, Li-Jun Tan","doi":"10.14336/AD.2024.1438","DOIUrl":"https://doi.org/10.14336/AD.2024.1438","url":null,"abstract":"Alzheimer's disease (AD) and osteoporosis (OP) are both age-related multifactorial degenerative diseases that share overlapping pathogenic mechanisms. While genetic factors contribute significantly to their onset and progression, environmental influences also play a crucial role. However, identifying the shared environmental factors and genetic architecture underlying the co-pathogenesis of AD and OP remains a significant challenge. This review highlights the common hormonal imbalances, environmental factors, genetic factors, and similar signaling pathways involved in both diseases. Furthermore, it explores the role of bone-secreted proteins and extracellular vesicles (EVs) in AD, as well as the effects of brain-derived proteins and EVs on bone homeostasis. By shedding light on the interconnected molecular and pathological mechanisms of AD and OP, this review aims to enhance our understanding of the underlying pathological molecular mechanisms of AD and OP, promote early diagnosis, and support the development of innovative therapeutic strategies for AD and OP patients.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Sarcopenia and Cognitive Decline in Hospitalized Older Adults from a Prospective Study. 来自一项前瞻性研究的住院老年人肌肉减少症和认知能力下降。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-23 DOI: 10.14336/AD.2024.1676

Sapir Kon-Kfir, Tali Cukierman-Yaffe, Haim Krupkin, Ana Belkin, Gadi Shlomai, Jonathan Bleier, Shiri Weinstein, Liora Bruckmayer, Elad Prinz, Alon Kaplan, Michal Goldenberg Shraga, Dana Lev, Shahar Dekel, Noa Shalmon, Nurit Tsarfaty, Niv Reiss, Evelyne Bischof, Avshalom Leibowitz

{"title":"Sarcopenia and Cognitive Decline in Hospitalized Older Adults from a Prospective Study.","authors":"Sapir Kon-Kfir, Tali Cukierman-Yaffe, Haim Krupkin, Ana Belkin, Gadi Shlomai, Jonathan Bleier, Shiri Weinstein, Liora Bruckmayer, Elad Prinz, Alon Kaplan, Michal Goldenberg Shraga, Dana Lev, Shahar Dekel, Noa Shalmon, Nurit Tsarfaty, Niv Reiss, Evelyne Bischof, Avshalom Leibowitz","doi":"10.14336/AD.2024.1676","DOIUrl":"https://doi.org/10.14336/AD.2024.1676","url":null,"abstract":"As populations age, sarcopenia increasingly impacts healthcare due to its associations with morbidity, mortality, and cognitive decline. This study is a cross-sectional analysis of prospectively collected data from 140 older adults hospitalized in an internal medicine department. Sarcopenia was measured by handgrip strength, and cognitive function by the Digit Symbol Substitution Test (DSST). Sarcopenic patients (n=78) had lower DSST scores (p=0.003) and Norton scores (p&;lt0.001) compared to non-sarcopenic patients. Handgrip strength showed a significant positive correlation with DSST scores (R=0.26, p=0.0019), persisting after adjustments for age and sex (R=0.42, p=1.7e-07). This study underscores a significant association between sarcopenia and cognitive decline in hospitalized older adults, advocating for routine sarcopenia and cognitive assessments upon admission. These findings emphasize the importance of identifying at-risk patients early and developing targeted interventions. Future research should further explore underlying mechanisms and validate findings in broader cohorts.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

The Flip Side of the Coin: METTL3 Serves as a Novel Cellular Senescence Accelerator via Negative Regulation of ITGA9. 硬币的另一面：METTL3通过负调控ITGA9作为一种新的细胞衰老加速器。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-20 DOI: 10.14336/AD.2024.1715

Yuting Li, Linying Huang, Miaochun Fang, Liwen Ye, Haiqing Yang, Weijia Wu, Yuan Yuan, Kun Cao, Hui-Ling Zheng, Xuerong Sun, Yun Wu, Xing-Dong Xiong, Xinguang Liu, Shun Xu

{"title":"The Flip Side of the Coin: METTL3 Serves as a Novel Cellular Senescence Accelerator via Negative Regulation of ITGA9.","authors":"Yuting Li, Linying Huang, Miaochun Fang, Liwen Ye, Haiqing Yang, Weijia Wu, Yuan Yuan, Kun Cao, Hui-Ling Zheng, Xuerong Sun, Yun Wu, Xing-Dong Xiong, Xinguang Liu, Shun Xu","doi":"10.14336/AD.2024.1715","DOIUrl":"https://doi.org/10.14336/AD.2024.1715","url":null,"abstract":"N6-Methyladenosine (m6A), a prevalent and dynamically regulated chemical modification, has recently emerged as a crucial post-transcriptional regulator of gene expression, and affected diverse eukaryotic biological processes. However, the role of m6A modification in aging research was still rarely reported. Herein, we uncovered that both the m6A modification level and the expression level of the methyltransferase METTL3 were significantly elevated during the aging process, as observed in the physiological aging mouse model in vivo, and the cellular senescence model in vitro. Furthermore, the silencing of METTL3 staved off the senescent phenotype of MEF cells, as evidenced by the downregulation of p16, decreased β-galactosidase activity and enhanced cell proliferative capacity, while METTL3 overexpression accelerated cellular senescence. Subsequently, a METTL3 transgenic mouse was generated, which exhibited a more pronounced senescence phenotype and a shortened lifespan. To deepen into the understanding of the molecular mechanisms of m6A and METTL3 in the aging process, high-throughput MeRIP sequencing was performed on young and senescent MEFs, and identified ITGA9 as a critical downstream m6A target, which might be negatively regulated by m6A modification or METTL3 through translation inhibition. And loss- or gain-of-function experiments unveiled that ITGA9 remarkably delayed the senescence of MEF cells. Additionally, the inhibition of ITGA9 reversed the impact of METTL3 silencing on delaying senescence, while ITGA9 overexpression counteracted the effect of ectopic expression of METTL3 on advancing cellular senescence. In aggregate, our data suggested that METTL3 promoted cellular senescence by m6A-dependent translational suppression of ITGA9, which was of great significance to alleviate the organismal aging process and age-related diseases.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735531","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Biological Aging in Combination with Lifestyle Factors in the Blood-Based Methylome: A Biomarker for Colorectal Cancer Susceptibility in African American Women. 血液甲基化组中生物衰老与生活方式因素的结合：非洲裔美国妇女结直肠癌易感性的生物标志物

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-19 DOI: 10.14336/AD.2025.0099

Su Yon Jung, Matteo Pellegrini, Herbert Yu

{"title":"Biological Aging in Combination with Lifestyle Factors in the Blood-Based Methylome: A Biomarker for Colorectal Cancer Susceptibility in African American Women.","authors":"Su Yon Jung, Matteo Pellegrini, Herbert Yu","doi":"10.14336/AD.2025.0099","DOIUrl":"https://doi.org/10.14336/AD.2025.0099","url":null,"abstract":"DNA methylation (DNAm)-based estimators of age are highly accurate for biological aging in multiple tissues, but their functional roles remain poorly understood in colorectal cancer (CRC), an age-related disease whose burden is higher in aged African Americans (AAs) than in whites. A greater rate of epigenetic age deviation from chronologic age was observed in AAs' colorectal tissues than in whites', emphasizing AA-specific investigation for epigenetic aging in CRC. Tumor tissue-based DNAm exclusively reflects cancerization, raising a question about its cancer predictability. A prediagnostic peripheral blood leukocyte (PBL)-based DNAm aging marker may thus provide keys to CRC etiology and prevention. From the largest study cohort, we examined 621 AA postmenopausal women 50-79 years old, including a subset of 14 who developed CRC, with their prediagnostic PBL-DNAm. Using three well-known pan-tissue- and blood-based epigenetic clocks, we evaluated correlations with CRC risk and to what degree the cancer risk is modified by lifestyle factors. Epigenetically older age and increased age acceleration were associated with reduced risk for CRC development. Of note, when women had accelerated aging phenotypes at screening, a substantial increased CRC risk was observed in short-term users of exogeneous estrogen, while a profound risk reduction was shown in women eating a healthy diet. Our study contributes to better understanding of the exertion of lifestyle factors in combination with methylome-based aging in colorectal carcinogenesis, detecting a prediagnostic PBL-based aging biomarker that promotes epigenetically targeted strategies tailored to aged AA women at high risk.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Towards Precision Aging Biology: Single-Cell Multi-Omics and Advanced AI-Driven Strategies. 迈向精确衰老生物学：单细胞多组学和先进的人工智能驱动策略。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-17 DOI: 10.14336/AD.2025.0218

Sijia Xie, Xinwei Luo, Feitong Hong, Yijie Wei, Yuduo Hao, Xueqin Xie, Xiaolong Li, Guangbo Xie, Fuying Dao, Hao Lyu

{"title":"Towards Precision Aging Biology: Single-Cell Multi-Omics and Advanced AI-Driven Strategies.","authors":"Sijia Xie, Xinwei Luo, Feitong Hong, Yijie Wei, Yuduo Hao, Xueqin Xie, Xiaolong Li, Guangbo Xie, Fuying Dao, Hao Lyu","doi":"10.14336/AD.2025.0218","DOIUrl":"https://doi.org/10.14336/AD.2025.0218","url":null,"abstract":"Individual aging is a complex biological process involving multiple levels, with molecular changes existing in heterogeneity across different cell types and tissues, being regulated by both internal and external factors. Traditional senescence markers, including p16, cell morphological changes, and cell cycle arrest, can only partially reflect the complexity of senescence. Single-cell omics technology facilitates the integration of multi-faceted data, including gene expression profiles, spatial dynamics, chromatin accessibility and metabolic pathways. This comprehensive approach enhances the development of biomarkers, granting us a more profound insight into the heterogeneity inherent within senescent cell populations. In this review, we summarize the application of single cell multi-omics approaches in analyzing senescence mechanisms and potential intervention targets from the perspectives of transcriptomics, epigenetics, metabolomics, and proteomics, explore the potential of developing new senescence markers at the cellular level using machine learning algorithms and artificial intelligence in bioinformatics analysis. Finally, we further discuss the challenges and prospective trajectories within this research domain to provide a more comprehensive perspective on dissecting the regulatory networks of senescence cells.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735532","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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

Targeting T-cell Aging to Remodel the Aging Immune System and Revitalize Geriatric Immunotherapy. 靶向t细胞老化，重塑老化免疫系统，振兴老年免疫治疗。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-15 DOI: 10.14336/AD.2025.0061

Mi Chen, Zhou Su, Jianxin Xue

引用次数: 0

Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets. 脓毒症的免疫衰老：分子机制和潜在的治疗靶点。

IF 7 2区医学

Aging and Disease Pub Date : 2025-03-14 DOI: 10.14336/AD.2025.0039

Heyang Sun, Qianya Hong, Chenning Li, Shuainan Zhu, Ying Yu, Hao Zhang, Kefang Guo

{"title":"Immunosenescence in Sepsis: Molecular Mechanisms and Potential Therapeutic Targets.","authors":"Heyang Sun, Qianya Hong, Chenning Li, Shuainan Zhu, Ying Yu, Hao Zhang, Kefang Guo","doi":"10.14336/AD.2025.0039","DOIUrl":"https://doi.org/10.14336/AD.2025.0039","url":null,"abstract":"Sepsis is a systemic inflammatory response triggered by infection that can result in immune regulation disruption and organ dysfunction. As an individual age, a phenomenon known as immunosenescence occurs. Immunosenescence is characterized by the deterioration of immune cells and organs. This decline leads to immune dysfunction, which is closely associated with an increased mortality rate among elderly sepsis patients. Recent studies have revealed that various responses during sepsis can induce premature aging of immune organs and cells in younger individuals, a process referred to as premature immunosenescence, which further accelerates the progression of sepsis and contributes to adverse outcomes. There is a significant correlation between immunosenescence and sepsis; therefore, understanding the specific manifestations and underlying mechanisms of immunosenescence induced by sepsis is imperative. Additionally, treatment strategies aimed at reversing or alleviating both immune aging and immune suppression in septic patients are worthwhile exploring and will also improve understanding of the concept of immunosenescence.","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143735630","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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