Biogerontology最新文献

{"title":"Cell-type specific and differential expression of LINC-RSAS long noncoding RNA declines in the testes during ageing of the rat.","authors":"Ajay Kumar Danga, Sukhleen Kour, Anita Kumari, Pramod C Rath","doi":"10.1007/s10522-023-10088-1","DOIUrl":"10.1007/s10522-023-10088-1","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have emerged as major regulators of gene expression, chromatin structure, epigenetic changes, post-transcriptional processing of RNAs, translation of mRNAs into proteins as well as contributing to the process of ageing. Ageing is a universal, slow, progressive change in almost all physiological processes of organisms after attaining reproductive maturity and often associated with age-related diseases. Mammalian testes contain various cell-types, vast reservoir of transcriptome complexity, produce haploid male gametes for reproduction and testosterone for development and maintenance of male sexual characters as well as contribute genetic variation to the species. We report age-related decline in expression and cellular localization of Long intergenic noncoding repeat-rich sense-antisense (LINC-RSAS) RNA in the testes and its major cell-types such as primary spermatocytes, Leydig cells and Sertoli cells during ageing of the rat. LINC-RSAS expression in testes increased from immature (4-weeks) to adult (16- and 44-weeks) and declined from adult (44-weeks) to nearly-old (70-weeks) rats. Genomic DNA methylation in the testes showed a similar pattern. Cell-type specific higher expression of LINC-RSAS was observed in primary spermatocytes (pachytene cells), Leydig cells and Sertoli cells of testes of adult rats. Over-expression of LINC-RSAS in cultured human cell lines revealed its possible role in cell-cycle control and apoptosis. We propose that LINC-RSAS expression is involved in molecular physiology of primary spermatocytes, Leydig cells and Sertoli cells of adult testes and its decline is associated with diminishing function of testes during ageing of the rat.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"543-566"},"PeriodicalIF":4.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139728851","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}

{"title":"Berberis vulgaris L. extract supplementation exerts regulatory effects on the lifespan and healthspan of Drosophila through its antioxidant activity depending on the sex.","authors":"Denis Golubev, Elena Platonova, Nadezhda Zemskaya, Oksana Shevchenko, Mikhail Shaposhnikov, Polina Nekrasova, Sergey Patov, Umida Ibragimova, Nikita Valuisky, Alexander Borisov, Xenia Zhukova, Svetlana Sorokina, Roman Litvinov, Alexey Moskalev","doi":"10.1007/s10522-023-10083-6","DOIUrl":"10.1007/s10522-023-10083-6","url":null,"abstract":"<p><p>Worldwide the aging population continues to increase, so the concept of healthy longevity medicine has become increasingly significant in modern society. Berberis vulgaris L. fruits serve as a functional food supplement with a high concentration of bioactive compounds, which offer numerous health-promoting benefits. The goal of this study was to investigate the geroprotective effect of Berberis vulgaris L. extract. Here we show that extract of Berberis vulgaris L. can, depending on concentrate, increases lifespan up to 6%, promote healthspan (stress resistance up to 35%, locomotor activity up to 25%, integrity of the intestinal barrier up to 12%, metabolic rate up to 5%) of Drosophila melanogaster (in vitro) and exhibits antioxidant (using red blood cell tests) and antiglycation activity (using glycation of bovine serum albumin) (in vitro). In addition to this, the extract does not exhibit cytotoxic properties in vitro, unlike the well-known polyphenolic compound quercetin. qRT-PCR has revealed the involvement of metabolic, heat shock response and lipid metabolism genes in the observed effects.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"507-528"},"PeriodicalIF":4.5,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139039458","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}

{"title":"\"Slight chemical damage due to drinking modest amount of sake, might induce beneficial effects\" as a form of hormesis: an interview with Professor Sataro Goto.","authors":"Zsolt Radak","doi":"10.1007/s10522-023-10069-4","DOIUrl":"10.1007/s10522-023-10069-4","url":null,"abstract":"<p><p>Professor Sataro Goto is one of the pioneers of biological aging research in Japan. He is renowned for his work on the role of protein errors and modifications, the accumulation of abnormal proteins due to reduced protein turnover, and the modulation of aging and lifespan by adult-onset dietary restriction and regular exercise. Professor Goto is a remarkably intelligent, visionary, empathetic, humble, and wise man, who kindly agreed to this interview that I (Zsolt Radak) made with him during one of my frequent visits to his labs, in February 2023.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"415-422"},"PeriodicalIF":4.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11142996/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"50160542","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}

{"title":"Investigation of anti-aging and anti-infection properties of Jingfang Granules using the Caenorhabditis elegans model.","authors":"Xin Yin, Yiwei Meng, Chenghong Sun, Yanqiu Zhao, Weitao Wang, Peipei Zhao, Mengmeng Wang, Jingli Ren, Jingchun Yao, Lixin Zhang, Xuekui Xia","doi":"10.1007/s10522-023-10058-7","DOIUrl":"10.1007/s10522-023-10058-7","url":null,"abstract":"<p><p>Jingfang Granule (JFG), a traditional Chinese medicine, is frequently employed in clinical settings for the treatment of infectious diseases. Nevertheless, the anti-aging and anti-infection effects of JFG remain uncertain. In the present study, these effects were evaluated using the Caenorhabditis elegans (C. elegans) N2 as a model organism. The results demonstrated that JFG significantly increased the median lifespan of C. elegans by 31.2% at a dosage of 10 mg/mL, without any discernible adverse effects, such as alterations in the pharyngeal pumping rate or nematode motility. Moreover, JFG notably increased oviposition by 11.3%. Subsequent investigations revealed that JFG enhanced oxidative stress resistance in C. elegans by reducing reactive oxygen species levels and significantly improved survival rates in nematodes infected with Pseudomonas aeruginosa ATCC 9027. These findings suggest that JFG delays reproductive senescence in C. elegans and protects them from oxidative stress, thereby extending their lifespan. Additionally, JFG improves the survival of P. aeruginosa-infected nematodes. Consequently, JFG has potential as a candidate for the development of anti-aging and anti-infection functional medicines.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"433-445"},"PeriodicalIF":4.5,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9981966","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}

{"title":"Renal aging and mitochondrial quality control.","authors":"Xiuli Guo, Jiao Wang, Yinjie Wu, Xinwang Zhu, Li Xu","doi":"10.1007/s10522-023-10091-6","DOIUrl":"10.1007/s10522-023-10091-6","url":null,"abstract":"<p><p>Mitochondria are dynamic organelles that participate in different cellular process that control metabolism, cell division, and survival, and the kidney is one of the most metabolically active organs that contains abundant mitochondria. Perturbations in mitochondrial homeostasis in the kidney can accelerate kidney aging, and maintaining mitochondrial homeostasis can effectively delay aging in the kidney. Kidney aging is a degenerative process linked to detrimental processes. The significance of aberrant mitochondrial homeostasis in renal aging has received increasing attention. However, the contribution of mitochondrial quality control (MQC) to renal aging has not been reviewed in detail. Here, we generalize the current factors contributing to renal aging, review the alterations in MQC during renal injury and aging, and analyze the relationship between mitochondria and intrinsic renal cells. We also introduce MQC in the context of renal aging, and discuss the study of mitochondria in the intrinsic cells of the kidney, which is the innovation of our paper. In addition, during kidney injury and repair, the specific functions and regulatory mechanisms of MQC systems in resident and circulating cell types remain unclear. Currently, most of the studies we reviewed are based on animal and cellular models, the relationship between renal tissue aging and mitochondria has not been adequately investigated in clinical studies, and there is still a long way to go.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"399-414"},"PeriodicalIF":4.5,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139721434","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}

{"title":"An underappreciated peculiarity of late-life human mortality kinetics assessed through the lens of a generalization of the Gompertz-Makeham law.","authors":"A Golubev","doi":"10.1007/s10522-023-10079-2","DOIUrl":"10.1007/s10522-023-10079-2","url":null,"abstract":"<p><p>Much attention in biogerontology is paid to the deceleration of mortality rate increase with age by the end of a species-specific lifespan, e.g. after ca. 90 years in humans. Being analyzed based on the Gompertz law µ(t)=µ₀e^γt with its inbuilt linearity of the dependency of lnµ on t, this is commonly assumed to reflect the heterogeneity of populations where the frailer subjects die out earlier thus increasing the proportions of those whose dying out is slower and leading to decreases in the demographic rates of aging. Using Human Mortality Database data related to France, Sweden and Japan in five periods 1920, 1950, 1980, 2018 and 2020 and to the cohorts born in 1920, it is shown by LOESS smoothing of the lnµ-vs-t plots and constructing the first derivatives of the results that the late-life deceleration of the life-table aging rate (LAR) is preceded by an acceleration. It starts at about 65 years and makes LAR at about 85 years to become 30% higher than it was before the acceleration. Thereafter, LAR decreases and reaches the pre-acceleration level at ca. 90 years. This peculiarity cannot be explained by the predominant dying out of frailer subjects at earlier ages. Its plausible explanation may be the acceleration of the biological aging in humans at ages above 65-70 years, which conspicuously coincide with retirement. The decelerated biological aging may therefore contribute to the subsequent late-life LAR deceleration. The biological implications of these findings are discussed in terms of a generalized Gompertz-Makeham law µ(t) = C(t)+µ₀e^f(t).</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"479-490"},"PeriodicalIF":4.5,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138440274","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}

{"title":"Targeting the epigenetically older individuals for geroprotective trials: the use of DNA methylation clocks.","authors":"Elena Sandalova, Andrea B Maier","doi":"10.1007/s10522-023-10077-4","DOIUrl":"10.1007/s10522-023-10077-4","url":null,"abstract":"<p><p>Chronological age is the most important risk factor for the incidence of age-related diseases. The pace of ageing determines the magnitude of that risk and can be expressed as biological age. Targeting fundamental pathways of human aging with geroprotectors has the potential to lower the biological age and therewith prolong the healthspan, the period of life one spends in good health. Target populations for geroprotective interventions should be chosen based on the ageing mechanisms being addressed and the expected effect of the geroprotector on the primary outcome. Biomarkers of ageing, such as DNA methylation age, can be used to select populations for geroprotective interventions and as a surrogate outcome. Here, the use of DNA methylation clocks for selecting target populations for geroprotective intervention is explored.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":" ","pages":"423-431"},"PeriodicalIF":4.4,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134648413","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}

{"title":"Altered lactate/pyruvate ratio may be responsible for aging-associated intestinal barrier dysfunction in male rats","authors":"Berrin Papila, Ayla Karimova, Ilhan Onaran","doi":"10.1007/s10522-024-10102-0","DOIUrl":"https://doi.org/10.1007/s10522-024-10102-0","url":null,"abstract":"<p>Some evidence points to a link between aging-related increased intestinal permeability and mitochondrial dysfunction in in-vivo models. Several studies have also demonstrated age-related accumulation of the of specific deletion 4834-bp of “common” mitochondrial DNA (mtDNA) in various rat tissues and suggest that this deletion may disrupt mitochondrial metabolism. The present study aimed to investigate possible associations among the mitochondrial DNA (mtDNA) common deletion, mitochondrial function, intestinal permeability, and aging in rats. The study was performed on the intestinal tissue from (24 months) and young (4 months) rats. mtDNA4834 deletion, mtDNA copy number, mitochondrial membrane potential, and ATP, lactate and pyruvate levels were analyzed in tissue samples. Zonulin and intestinal fatty acid-binding protein (I-FABP) levels were also evaluated in serum. Serum zonulin and I-FABP levels were significantly higher in 24-month-old rats than 4-month-old rats (<i>p</i> = 0.04, <i>p</i> = 0.026, respectively). There is not significant difference in mtDNA4834 copy levels was observed between the old and young intestinal tissues (<i>p</i> &gt; 0.05). The intestinal mitochondrial DNA copy number was similar between the two age groups (<i>p</i> &gt; 0.05). No significant difference was observed in ATP levels in the intestinal tissue lysates between old and young rats (<i>p</i> &gt; 0.05). ATP levels in isolated mitochondria from both groups were also similar. Analysis of MMP using JC-10 in intestinal tissue mitochondria showed that mitochondrial membrane potentials (red/green ratios) were similar between the two age groups (<i>p</i> &gt; 0.05). Pyruvate tended to be higher in the 24-month-old rat group and the L/P ratio was found to be approximately threefold lower in the intestinal tissue of the older rats compared to the younger rats (<i>p</i> &lt; 0.002). The tissue lactate/pyruvate ratio (L/P) was three times lower in old rats than in young rats. Additionally, there were significant negative correlations between intestinal permeability parameters and L/P ratios. The intestinal tissues of aged rats are not prone to accumulate mtDNA common deletion, we suggest that this mutation does not explain the age-related increase in intestinal permeability. It seems to be more likely that altered glycolytic capacity could be a link to increased intestinal permeability with age. This observation strengthens assertions that the balance between glycolysis and mitochondrial metabolism may play a critical role in intestinal barrier functions.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"2018 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140590949","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}

{"title":"Combined dasatinib and quercetin treatment contributes to skin rejuvenation through selective elimination of senescent cells in vitro and in vivo","authors":"Kento Takaya, Kazuo Kishi","doi":"10.1007/s10522-024-10103-z","DOIUrl":"https://doi.org/10.1007/s10522-024-10103-z","url":null,"abstract":"<p>The skin’s protective functions are compromised over time by both endogenous and exogenous aging. Senescence is well-documented in skin phenotypes, such as wrinkling and sagging, a consequence of the senescence-associated secretory phenotype (SASP) that involves the accumulation of senescent fibroblasts, chronic inflammation, and collagen remodeling. Although therapeutic approaches for eliminating senescent cells from the skin are available, their efficacy remains unclear. Accordingly, we aimed to examine the effects of dasatinib in combination with quercetin (D + Q) on senescent human skin fibroblasts and aging human skin. Senescence was induced in human dermal fibroblasts (HDFs) using approaches such as long-term passaging, ionizing radiation, and doxorubicin treatment. The generated senescent cells were treated with D + Q or vehicle. Additionally, a mouse-human chimera model was generated by subcutaneously transplanting whole-skin grafts of aged individuals onto nude mice. Mouse models were administered D + Q or vehicle by oral gavage for 30 days. Subsequently, skin samples were harvested and stained for senescence-associated beta-galactosidase. Senescence-associated markers were assessed by western blotting, reverse transcription-quantitative PCR and histological analyses. Herein, D + Q selectively eliminated senescent HDFs in all cellular models of induced senescence. Additionally, D + Q-treated aged human skin grafts exhibited increased collagen density and suppression of the SASP compared with control grafts. No adverse events were observed during the study period. Collectively, D + Q could ameliorate skin aging through selective elimination of senescent dermal fibroblasts and suppression of the SASP. Our findings suggest that D + Q could be developed as an effective therapeutic approach for combating skin aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"21 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140591061","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}

{"title":"RNA-sequencing exploration on SIR2 and SOD genes in Polyalthia longifolia leaf methanolic extracts (PLME) mediated anti-aging effects in Saccharomyces cerevisiae BY611 yeast cells","authors":"Manisekaran Hemagirri, Yeng Chen, Subash C. B. Gopinath, Mohd Adnan, Mitesh Patel, Sreenivasan Sasidharan","doi":"10.1007/s10522-024-10104-y","DOIUrl":"https://doi.org/10.1007/s10522-024-10104-y","url":null,"abstract":"<p><i>Polyalthia longifolia</i> is well-known for its abundance of polyphenol content and traditional medicinal uses. Previous research has demonstrated that the methanolic extract of <i>P. longifolia</i> leaves (PLME, 1 mg/mL) possesses anti-aging properties in <i>Saccharomyces cerevisiae</i> BY611 yeast cells. Building on these findings, this study delves deeper into the potential antiaging mechanism of PLME, by analyzing the transcriptional responses of BY611 cells treated with PLME using RNA-sequencing (RNA-seq) technology. The RNA-seq analysis results identified 1691 significantly (padj &lt; 0.05) differentially expressed genes, with 947 upregulated and 744 downregulated genes. Notably, the expression of three important aging-related genes, <i>SIR2</i>, <i>SOD1</i>, and <i>SOD2</i>, showed a significant difference following PLME treatment. The subsequent integration of these targeted genes with GO and KEGG pathway analysis revealed the multifaceted nature of PLME’s anti-aging effects in BY611 yeast cells. Enriched GO and KEGG analysis showed that PLME treatment promotes the upregulation of <i>SIR2</i>, <i>SOD1</i>, and <i>SOD2</i> genes, leading to a boosted cellular antioxidant defense system, reduced oxidative stress, regulated cell metabolism, and maintain genome stability. These collectively increased longevities in PLME-treated BY611 yeast cells and indicate the potential anti-aging action of PLME through the modulation of <i>SIR2</i> and <i>SOD</i> genes. The present study provided novel insights into the roles of <i>SIR2</i>, <i>SOD1</i>, and <i>SOD2</i> genes in the anti-aging effects of PLME treatment, offering promising interventions for promoting healthy aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"38 1","pages":""},"PeriodicalIF":4.5,"publicationDate":"2024-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140591069","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}