Biogerontology最新文献_第8页

Linking telomere dynamics to evolution, life history and environmental change: perspectives, predictions and problems. 将端粒动态与进化、生活史和环境变化联系起来：观点、预测和问题。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-04-01 Epub Date: 2024-01-22 DOI: 10.1007/s10522-023-10081-8

Pat Monaghan

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Telomeres and telomerase: active but complex players in life-history decisions. 端粒和端粒酶：生命史决策中活跃而复杂的角色。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-04-01 Epub Date: 2023-08-23 DOI: 10.1007/s10522-023-10060-z

Radmila Čapková Frydrychová, Barbora Konopová, Vratislav Peska, Miloslav Brejcha, Michala Sábová

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Methods that shaped telomerase research. 影响端粒酶研究的方法。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-04-01 Epub Date: 2023-10-31 DOI: 10.1007/s10522-023-10073-8

Louise Bartle, Raymund J Wellinger

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Mitochondria and telomeres: hand in glove. 线粒体和端粒：携手合作。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-04-01 Epub Date: 2023-10-21 DOI: 10.1007/s10522-023-10074-7

Mélina Vaurs, Elif Beyza Dolu, Anabelle Decottignies

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Alexey Olovnikov: theoretical biology beyond the margins. 阿列克谢-奥洛夫尼科夫：超越边缘的理论生物学。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-04-01 Epub Date: 2023-09-07 DOI: 10.1007/s10522-023-10061-y

Ivan A Olovnikov

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The potential use of nanozyme in aging and age‐related diseases 纳米酶在衰老和老年相关疾病中的潜在用途

IF 4.5 4区医学

Biogerontology Pub Date : 2024-03-11 DOI: 10.1007/s10522-024-10095-w

Amirsasan Gorgzadeh, Paria Arab Amiri, Saman Yasamineh, Basim Kareem Naser, Khairia abdulrahman abdulallah

{"title":"The potential use of nanozyme in aging and age‐related diseases","authors":"Amirsasan Gorgzadeh, Paria Arab Amiri, Saman Yasamineh, Basim Kareem Naser, Khairia abdulrahman abdulallah","doi":"10.1007/s10522-024-10095-w","DOIUrl":"https://doi.org/10.1007/s10522-024-10095-w","url":null,"abstract":"<p>The effects of an increasingly elderly population are among the most far-reaching in 21st-century society. The growing healthcare expense is mainly attributable to the increased incidence of chronic illnesses that accompany longer life expectancies. Different ideas have been put up to explain aging, but it is widely accepted that oxidative damage to proteins, lipids, and nucleic acids contributes to the aging process. Increases in life expectancy in all contemporary industrialized cultures are accompanied by sharp increases in the prevalence of age-related diseases such as cardiovascular and neurological conditions, type 2 diabetes, osteoporosis, and cancer. Therefore, academic and public health authorities should prioritize the development of therapies to increase health span. Nanozyme (NZ)-like activity in nanomaterials has been identified as promising anti-aging nanomedicines. More than that, nanomaterials displaying catalytic activities have evolved as artificial enzymes with high structural stability, variable catalytic activity, and functional diversity for use in a wide range of biological settings, including those dealing with age-related disorders. Due to their inherent enzyme-mimicking qualities, enzymes have attracted significant interest in treating diseases associated with reactive oxygen species (ROS). The effects of NZs on aging and age-related disorders are summarized in this article. Finally, prospects and threats to enzyme research and use in aging and age-related disorders are offered.</p><h3 data-test=\"abstract-sub-heading\">Graphical Abstract</h3>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"079 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140099036","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway SGLT2抑制剂empagliflozin通过AMPKα/MMP9/TGF-β1/Smad途径抑制自然衰老雄性小鼠的骨骼肌纤维化

IF 4.5 4区医学

Biogerontology Pub Date : 2024-02-26 DOI: 10.1007/s10522-024-10093-y

{"title":"The SGLT2 inhibitor empagliflozin inhibits skeletal muscle fibrosis in naturally aging male mice through the AMPKα/MMP9/TGF-β1/Smad pathway","authors":"","doi":"10.1007/s10522-024-10093-y","DOIUrl":"https://doi.org/10.1007/s10522-024-10093-y","url":null,"abstract":"<h3>Abstact</h3> <p>With advancing age, the incidence of sarcopenia increases, eventually leading to a cascade of adverse events. However, there is currently a lack of effective pharmacological treatment for sarcopenia. Sodium-glucose co-transporter 2 inhibitor (SGLT2i) empagliflozin demonstrates anti-fibrotic capabilities in various organs. This study aims to determine whether empagliflozin can improve skeletal muscle fibrosis induced by sarcopenia in naturally aging mice. A natural aging model was established by feeding male mice from 13 months of age to 19 months of age. A fibrosis model was created by stimulating skeletal muscle fibroblasts with TGF-β1. The Forelimb grip strength test assessed skeletal muscle function, and expression levels of COL1A1, COL3A1, and α-SMA were analyzed by western blot, qPCR, and immunohistochemistry. Additionally, levels of AMPKα/MMP9/TGFβ1/Smad signaling pathways were examined. In naturally aging mice, skeletal muscle function declines, expression of muscle fibrosis markers increases, AMPKα expression is downregulated, and MMP9/TGFβ1/Smad signaling pathways are upregulated. However, treatment with empagliflozin reverses this phenomenon. At the cellular level, empagliflozin exhibits similar anti-fibrotic effects, and these effects are attenuated by Compound C and siAMPKα. Empagliflozin exhibits anti-fibrotic effects, possibly associated with the AMPK/MMP9/TGFβ1/Smad signaling pathways.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"18 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139968080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

A CRISPR base editing approach for the functional assessment of telomere biology disorder-related genes in human health and aging 用 CRISPR 碱基编辑方法对人类健康和衰老过程中端粒生物学紊乱相关基因进行功能评估

IF 4.5 4区医学

Biogerontology Pub Date : 2024-02-04 DOI: 10.1007/s10522-024-10094-x

Gustavo Borges, Yahya Benslimane, Lea Harrington

{"title":"A CRISPR base editing approach for the functional assessment of telomere biology disorder-related genes in human health and aging","authors":"Gustavo Borges, Yahya Benslimane, Lea Harrington","doi":"10.1007/s10522-024-10094-x","DOIUrl":"https://doi.org/10.1007/s10522-024-10094-x","url":null,"abstract":"<p>Telomere Biology Disorders (TBDs) are a group of rare diseases characterized by the presence of short and/or dysfunctional telomeres. They comprise a group of bone marrow failure syndromes, idiopathic pulmonary fibrosis, and liver disease, among other diseases. Genetic alterations (variants) in the genes responsible for telomere homeostasis have been linked to TBDs. Despite the number of variants already identified as pathogenic, an even more significant number must be better understood. The study of TBDs is challenging since identifying these variants is difficult due to their rareness, it is hard to predict their impact on the disease onset, and there are not enough samples to study. Most of our knowledge about pathogenic variants comes from assessing telomerase activity from patients and their relatives affected by a TBD. However, we still lack a cell-based model to identify new variants and to study the long-term impact of such variants on the genes involved in TBDs. Herein, we present a cell-based model using CRISPR base editing to mutagenize the endogenous alleles of 21 genes involved in telomere biology. We identified key residues in the genes encoding 17 different proteins impacting cell growth. We provide functional evidence for variants of uncertain significance in patients with TBDs. We also identified variants resistant to telomerase inhibition that, similar to cells expressing wild-type telomerase, exhibited increased tumorigenic potential using an in vitro tumour growth assay. We believe that such cell-based approaches will significantly advance our understanding of the biology of TBDs and may contribute to the development of new therapies for this group of diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"24 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139677882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

Fisetin, a potential skin rejuvenation drug that eliminates senescent cells in the dermis. Fisetin，一种潜在的皮肤再生药物，可以消除真皮中的衰老细胞。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-02-01 Epub Date: 2023-09-22 DOI: 10.1007/s10522-023-10064-9

Kento Takaya, Toru Asou, Kazuo Kishi

{"title":"Fisetin, a potential skin rejuvenation drug that eliminates senescent cells in the dermis.","authors":"Kento Takaya, Toru Asou, Kazuo Kishi","doi":"10.1007/s10522-023-10064-9","DOIUrl":"10.1007/s10522-023-10064-9","url":null,"abstract":"<p><p>Accumulation of senescent fibroblasts, chronic inflammation, and collagen remodeling due to aging-related secretory phenotypes have been hypothesized to cause age-related skin aging, which results in wrinkles and loss of skin elasticity, thus compromising appearance attractiveness. However, the rejuvenating effects of removing senescent cells from the human skin and the efficacy of related therapeutic agents remain unclear. Here, we investigated the effects of fisetin, a potential anti-aging component found in various edible fruits and vegetables, on senescent human dermal fibroblasts (HDFs) and aging human skin. Senescence was induced in primary HDFs using long-term passaging and treatment with ionizing radiation, and cell viability was assessed after treatment with fisetin and a control component. A mouse/human chimeric model was established by subcutaneously transplanting whole skin grafts from aged individuals into nude mice, which were treated intraperitoneally with fisetin or control a component for 30 d. Skin samples were obtained and subjected to senescence-associated-beta-galactosidase staining; the extent of aging was evaluated using western blotting, reverse transcription-quantitative PCR, and histological analysis. Fisetin selectively eliminated senescent dermal fibroblasts in both senescence-induced cellular models; this effect is attributable to cell death induction by caspases 3, 8, and 9-mediated endogenous and exogenous apoptosis. Fisetin-treated senescent human skin grafts showed increased collagen density and decreased senescence-associated secretory phenotypes (SASP), including matrix metalloproteinases and interleukins. No apparent adverse events were observed. Thus, fisetin could improve skin aging through selective removal of senescent dermal fibroblasts and SASP inhibition, indicating its potential as an effective novel therapeutic agent for combating skin aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"161-175"},"PeriodicalIF":4.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41095565","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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

AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration. AMPK信号抑制肌成纤维细胞分化：对年龄相关组织纤维化和变性的影响。

IF 4.5 4区医学

Biogerontology Pub Date : 2024-02-01 Epub Date: 2023-11-02 DOI: 10.1007/s10522-023-10072-9

Antero Salminen

{"title":"AMPK signaling inhibits the differentiation of myofibroblasts: impact on age-related tissue fibrosis and degeneration.","authors":"Antero Salminen","doi":"10.1007/s10522-023-10072-9","DOIUrl":"10.1007/s10522-023-10072-9","url":null,"abstract":"<p><p>Disruption of the extracellular matrix (ECM) and an accumulation of fibrotic lesions within tissues are two of the distinctive hallmarks of the aging process. Tissue fibroblasts are mesenchymal cells which display an impressive plasticity in the regulation of ECM integrity and thus on tissue homeostasis. Single-cell transcriptome studies have revealed that tissue fibroblasts exhibit a remarkable heterogeneity with aging and in age-related diseases. Excessive stress and inflammatory insults induce the differentiation of fibroblasts into myofibroblasts which are fusiform contractile cells and abundantly secrete the components of the ECM and proteolytic enzymes as well as many inflammatory mediators. Detrimental stresses can also induce the transdifferentiation of certain mesenchymal and myeloid cells into myofibroblasts. Interestingly, many age-related stresses, such as oxidative and endoplasmic reticulum stresses, ECM stiffness, inflammatory mediators, telomere shortening, and several alarmins from damaged cells are potent inducers of myofibroblast differentiation. Intriguingly, there is convincing evidence that the signaling pathways stimulated by the AMP-activated protein kinase (AMPK) are potent inhibitors of myofibroblast differentiation and accordingly AMPK signaling reduces fibrotic lesions within tissues, e.g., in age-related cardiac and pulmonary fibrosis. AMPK signaling is not only an important regulator of energy metabolism but it is also able to control cell fate determination and many functions of the immune system. It is known that AMPK signaling can delay the aging process via an integrated signaling network. AMPK signaling inhibits myofibroblast differentiation, e.g., by suppressing signaling through the TGF-β, NF-κB, STAT3, and YAP/TAZ pathways. It seems that AMPK signaling can alleviate age-related tissue fibrosis and degeneration by inhibiting the differentiation of myofibroblasts.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"83-106"},"PeriodicalIF":4.5,"publicationDate":"2024-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10794430/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71420348","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"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