Aging Biology最新文献_第2页

Restricting the Possibilities for Mechanisms of Calorie Restriction 限制热量限制机制的可能性

Aging Biology Pub Date : 2023-06-29 DOI: 10.59368/agingbio.20230006

Peter D. Adams

引用次数: 0

Analysis of Somatic Mutations in Senescent Cells Using Single-Cell Whole-Genome Sequencing 利用单细胞全基因组测序分析衰老细胞的体细胞突变

Aging Biology Pub Date : 2023-06-29 DOI: 10.59368/agingbio.20230007

A. Donato, Samuel I. Bloom, Eric Tuday, M. Islam, V. Gogulamudi, L. Lesniewski

引用次数: 0

Biology of Stress Responses in Aging. 老化过程中的压力反应生物学。

Aging Biology Pub Date : 2023-01-01 Epub Date: 2023-06-27 DOI: 10.59368/agingbio.20230001

Manolis Maragkakis, Sulochan Malla, Maria Hatzoglou, Aleksandra Trifunovic, Adam B Glick, Toren Finkel, Valter D Longo, Susmita Kaushik, Pura Muñoz-Cánoves, Gordon J Lithgow, Nirinjini Naidoo, Lauren N Booth, Matthew J Payea, Allison B Herman, Rafael de Cabo, David M Wilson, Luigi Ferrucci, Myriam Gorospe

{"title":"Biology of Stress Responses in Aging.","authors":"Manolis Maragkakis, Sulochan Malla, Maria Hatzoglou, Aleksandra Trifunovic, Adam B Glick, Toren Finkel, Valter D Longo, Susmita Kaushik, Pura Muñoz-Cánoves, Gordon J Lithgow, Nirinjini Naidoo, Lauren N Booth, Matthew J Payea, Allison B Herman, Rafael de Cabo, David M Wilson, Luigi Ferrucci, Myriam Gorospe","doi":"10.59368/agingbio.20230001","DOIUrl":"10.59368/agingbio.20230001","url":null,"abstract":"On April 28th, 2022, a group of scientific leaders gathered virtually to discuss molecular and cellular mechanisms of responses to stress. Conditions of acute, high-intensity stress are well documented to induce a series of adaptive responses that aim to promote survival until the stress has dissipated and then guide recovery. However, high-intensity or persistent stress that goes beyond the cell's compensatory capacity are countered with resilience strategies that are not completely understood. These adaptative strategies, which are an essential component of the study of aging biology, were the theme of the meeting. Specific topics discussed included mechanisms of proteostasis, such as the unfolded protein response (UPR) and the integrated stress response (ISR), as well as mitochondrial stress and lysosomal stress responses. Attention was also given to regulatory mechanisms and associated biological processes linked to age-related conditions, such as muscle loss and regeneration, cancer, senescence, sleep quality, and degenerative disease, with a general focus on the relevance of stress responses to frailty. We summarize the concepts and potential future directions that emerged from the discussion and highlight their relevance to the study of aging and age-related chronic diseases.","PeriodicalId":72130,"journal":{"name":"Aging Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10947073/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87282186","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aging, Parkinson's Disease, and Models: What Are the Challenges? 老龄化、帕金森病和模型：挑战是什么？

Aging Biology Pub Date : 2023-01-01 Epub Date: 2023-07-28 DOI: 10.59368/agingbio.20230010

Emily Rocha, Manish Chamoli, Shankar J Chinta, Julie K Andersen, Ruby Wallis, Erwan Bezard, Matt Goldberg, Tim Greenamyre, Warren Hirst, We-Li Kuan, Deniz Kirik, Laura Niedernhofer, Irit Rappley, Shalini Padmanabhan, Louis-Eric Trudeau, Maria Spillantini, Simon Scott, Lorenz Studer, Ilaria Bellantuono, Heather Mortiboys

{"title":"Aging, Parkinson's Disease, and Models: What Are the Challenges?","authors":"Emily Rocha, Manish Chamoli, Shankar J Chinta, Julie K Andersen, Ruby Wallis, Erwan Bezard, Matt Goldberg, Tim Greenamyre, Warren Hirst, We-Li Kuan, Deniz Kirik, Laura Niedernhofer, Irit Rappley, Shalini Padmanabhan, Louis-Eric Trudeau, Maria Spillantini, Simon Scott, Lorenz Studer, Ilaria Bellantuono, Heather Mortiboys","doi":"10.59368/agingbio.20230010","DOIUrl":"10.59368/agingbio.20230010","url":null,"abstract":"Parkinson's disease (PD) is a chronic, neurodegenerative condition characterized by motor symptoms such as bradykinesia, rigidity, and tremor, alongside multiple nonmotor symptoms. The appearance of motor symptoms is linked to progressive dopaminergic neuron loss within the substantia nigra. PD incidence increases sharply with age, suggesting a strong association between mechanisms driving biological aging and the development and progression of PD. However, the role of aging in the pathogenesis of PD remains understudied. Numerous models of PD, including cell models, toxin-induced models, and genetic models in rodents and nonhuman primates (NHPs), reproduce different aspects of PD, but preclinical studies of PD rarely incorporate age as a factor. Studies using patient neurons derived from stem cells via reprogramming methods retain some aging features, but their characterization, particularly of aging markers and reproducibility of neuron type, is suboptimal. Investigation of age-related changes in PD using animal models indicates an association, but this is likely in conjunction with other disease drivers. The biggest barrier to drawing firm conclusions is that each model lacks full characterization and appropriate time-course assessments. There is a need to systematically investigate whether aging increases the susceptibility of mouse, rat, and NHP models to develop PD and understand the role of cell models. We propose that a significant investment in time and resources, together with the coordination and sharing of resources, knowledge, and data, is required to accelerate progress in understanding the role of biological aging in PD development and improve the reliability of models to test interventions.","PeriodicalId":72130,"journal":{"name":"Aging Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11230631/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83049114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aging Rate Indicators: Speedometers for Aging Research in Mice. 衰老率指标:小鼠衰老研究的速度计。

Aging Biology Pub Date : 2023-01-01 DOI: 10.59368/agingbio.20230003

Richard A Miller, Xinna Li, Gonzalo Garcia

{"title":"Aging Rate Indicators: Speedometers for Aging Research in Mice.","authors":"Richard A Miller, Xinna Li, Gonzalo Garcia","doi":"10.59368/agingbio.20230003","DOIUrl":"https://doi.org/10.59368/agingbio.20230003","url":null,"abstract":"A \"biomarker of aging\" is conceptualized as an index of how far an individual has moved along the path from youth to old age. In contrast, an aging rate indicator (ARI) represents a measure of speed, rather than distance, that is, a measure of how rapidly the individual is moving toward the phenotypic changes typical of old age. This essay presents and reviews recent data suggesting common characteristics of slow-aging mice, whether the slowed aging is caused by a mutant allele, the calorie restriction diet, or drugs that slow aging and extend mean and maximal lifespan. Some of the candidate ARIs, shared by nine varieties of slow-aging mice, are physiological changes seen in fat, fat-associated macrophages, muscle, liver, brain, and plasma. Others are molecular measurements, reflecting activity of mTORC1, selective mRNA translation, or each of six MAP kinases in two distinct MAPK cascades in liver, muscle, or kidney. Changes in ARIs are notable in young adult mice after 8 months of drug or diet exposure, are detectable in mutant mice at least as early as 4-6 months of age, and persist until at least 18-22 months. Many of the candidate ARIs are thought to play an influential role in cognition, inflammation, exercise responses, and control of metabolic rate, and are thus plausible as modulators of age-related physiological and neurological illnesses. In principle, screening for drugs that induce alterations in ARIs in normal young adult mice might facilitate the search for preventive medicines that can retard aging and late-life illnesses in mice or in human populations.","PeriodicalId":72130,"journal":{"name":"Aging Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2023-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10486275/pdf/nihms-1928132.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10588057","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

Hallmarks of Aging: Causes and Consequences. 衰老的标志：原因与后果

Aging Biology Pub Date : 2023-01-01 DOI: 10.59368/agingbio.20230011

Dorota Skowronska-Krawczyk

引用次数: 0

FGF21 has a sex-specific role in calorie-restriction-induced beiging of white adipose tissue in mice. FGF21在卡路里限制诱导的小鼠白色脂肪组织粗化过程中具有性别特异性。

Aging Biology Pub Date : 2022-01-01

Mariah F Calubag, Ismail Ademi, Chung-Yang Yeh, Reji Babygirija, Heidi H Pak, Alyssa M Bhoopat, Ildiko Kasza, Cara L Green, Michelle M Sonsalla, Dudley W Lamming

{"title":"FGF21 has a sex-specific role in calorie-restriction-induced beiging of white adipose tissue in mice.","authors":"Mariah F Calubag, Ismail Ademi, Chung-Yang Yeh, Reji Babygirija, Heidi H Pak, Alyssa M Bhoopat, Ildiko Kasza, Cara L Green, Michelle M Sonsalla, Dudley W Lamming","doi":"","DOIUrl":"","url":null,"abstract":"Calorie restriction (CR) promotes healthspan and extends the lifespan of diverse organisms, including mice, and there is intense interest in understanding the molecular mechanisms by which CR functions. Some studies have demonstrated that CR induces fibroblast growth factor 21 (FGF21), a hormone that regulates energy balance and that when overexpressed, promotes metabolic health and longevity in mice, but the role of FGF21 in the response to CR has not been fully investigated. We directly examined the role of FGF21 in the physiological and metabolic response to a CR diet by feeding Fgf21-/- and wild-type control mice either ad libitum (AL) diet or a 30% CR diet for 15 weeks. Here, we find that FGF21 is largely dispensable for CR-induced improvements in body composition and energy balance, but that lack of Fgf21 blunts CR-induced changes aspects of glucose regulation and insulin sensitivity in females. Surprisingly, despite not affecting CR-induced changes in energy expenditure, loss of Fgf21 significantly blunts CR-induced beiging of white adipose tissue in male but not female mice. Our results shed new light on the molecular mechanisms involved in the beneficial effects of a CR diet, clarify that FGF21 is largely dispensable for the metabolic effects of a CR diet, and highlight a sex-dependent role for FGF21 in the molecular adaptation of white adipose tissue to CR.","PeriodicalId":72130,"journal":{"name":"Aging Biology","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10181818/pdf/nihms-1864795.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9873047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0