Senescence [Working Title]最新文献

Anti-Senescence Therapy Anti-Senescence疗法

Senescence [Working Title] Pub Date : 2022-02-02 DOI: 10.5772/intechopen.101585

Raghad Alshadidi

{"title":"Anti-Senescence Therapy","authors":"Raghad Alshadidi","doi":"10.5772/intechopen.101585","DOIUrl":"https://doi.org/10.5772/intechopen.101585","url":null,"abstract":"The development of therapeutic strategies aimed at the aging process of cells has attracted increasing attention in recent decades due to the involvement of this process in the development of many chronic and age-related diseases. Interestingly, preclinical studies have shown the success of a number of anti-aging approaches in the treatment of a range of chronic diseases. These approaches are directed against aging processes such as oxidative stress, telomerase shortening, inflammation, and deficient autophagy. Many strategies has been shown to be effective in delaying aging, including antiaging strategies based on establishing healthy lifestyle habits and pharmacological interventions aimed at disrupting senescent cells and senescent-associated secretory phenotype. Caloric restriction and intermittent fasting were reported to activate autophagy and reduce inflammation. In turn, immune-based strategies, senolytic agents, and senomorphics mediate their effects either by eliminating senescent cells through inducing apoptosis or by disrupting pathways by which senescent cells mediate their detrimental effects. In addition, given the association of the decline in the regenerative potential of stem cells with aging, many experimental and clinical studies indicate the effectiveness of stem cell transplantation in preventing or slowing the progress of age-related diseases by enhancing the repairing mechanisms and the secretion of many growth factors and cytokines.","PeriodicalId":419821,"journal":{"name":"Senescence [Working Title]","volume":"22 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2022-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"125344835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cellular Senescence in Bone 骨细胞衰老

Senescence [Working Title] Pub Date : 2021-12-28 DOI: 10.5772/intechopen.101803

Dan Wang, Haitao Wang

引用次数: 0

Identification of RNA Species That Bind to the hnRNP A1 in Normal and Senescent Human Fibroblasts 正常和衰老人类成纤维细胞中与hnRNP A1结合的RNA种类的鉴定

Senescence [Working Title] Pub Date : 2021-12-20 DOI: 10.5772/intechopen.101525

Heriberto Moran, Shanaz A. Ghandhi, N. Shimada, K. Hubbard

{"title":"Identification of RNA Species That Bind to the hnRNP A1 in Normal and Senescent Human Fibroblasts","authors":"Heriberto Moran, Shanaz A. Ghandhi, N. Shimada, K. Hubbard","doi":"10.5772/intechopen.101525","DOIUrl":"https://doi.org/10.5772/intechopen.101525","url":null,"abstract":"hnRNP A1 is a member of the hnRNPs (heterogeneous nuclear ribonucleoproteins) family of proteins that play a central role in regulating genes responsible for cell proliferation, DNA repair, apoptosis, and telomere biogenesis. Previous studies have shown that hnRNPA1 had reduced protein levels and increased cytoplasmic accumulation in senescent human diploid fibroblasts. The consequence of reduced protein expression and altered cellular localization may account for the alterations in gene expression observed during senescence. There is limited information for gene targets of hnRNP A1 as well as its in vivo function. In these studies, we performed RNA co-immunoprecipitation experiments using hnRNP A1 as the target protein to identify potential mRNA species in ribonucleoprotein (RNP) complexes. Using this approach, we identified the human double minute 2 (HDM2) mRNA as a binding target for hnRNP A1 in young and senescent human diploid fibroblasts cells. It was also observed that alterations of hnRNP A1 expression modulate HDM2 mRNA levels in young IMR-90 cells. We also demonstrated that the levels of HDM2 mRNA increased with the downregulation of hnRNP A1 and decrease with the overexpression of hnRNP A1. Although we did not observe a significant decrease in HDM2 protein level, a concomitant increase in p53 protein level was detected with the overexpression of hnRNP A1. Our studies also show that hnRNP A1 directly interacts with HDM2 mRNA at a region corresponding to its 3′ UTR (untranslated region of a gene). The results from this study demonstrate that hnRNP A1 has a novel role in participating in the regulation of HDM2 gene expression.","PeriodicalId":419821,"journal":{"name":"Senescence [Working Title]","volume":"262 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"115963994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic and Epigenetic Influences on Cutaneous Cellular Senescence 遗传和表观遗传对皮肤细胞衰老的影响

Senescence [Working Title] Pub Date : 2021-11-11 DOI: 10.5772/intechopen.101152

Tapash Jay Sarkar, Maiko Hermsmeier, Jessica L. Ross, G. Scott Herron

{"title":"Genetic and Epigenetic Influences on Cutaneous Cellular Senescence","authors":"Tapash Jay Sarkar, Maiko Hermsmeier, Jessica L. Ross, G. Scott Herron","doi":"10.5772/intechopen.101152","DOIUrl":"https://doi.org/10.5772/intechopen.101152","url":null,"abstract":"Skin is the largest human organ system, and its protective function is critical to survival. The epithelial, dermal, and subcutaneous compartments are heterogeneous mixtures of cell types, yet they all display age-related skin dysfunction through the accumulation of an altered phenotypic cellular state called senescence. Cellular senescence is triggered by complex and dynamic genetic and epigenetic processes. A senescence steady state is achieved in different cell types under various and overlapping conditions of chronological age, toxic injury, oxidative stress, replicative exhaustion, DNA damage, metabolic dysfunction, and chromosomal structural changes. These inputs lead to outputs of cell-cycle withdrawal and the appearance of a senescence-associated secretory phenotype, both of which accumulate as tissue pathology observed clinically in aged skin. This review details the influence of genetic and epigenetic factors that converge on normal cutaneous cellular processes to create the senescent state, thereby dictating the response of the skin to the forces of both intrinsic and extrinsic aging. From this work, it is clear that no single biomarker or process leads to senescence, but that it is a convergence of factors resulting in an overt aging phenotype.","PeriodicalId":419821,"journal":{"name":"Senescence [Working Title]","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"134251806","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0