Dataset Information

Deciphering aging-related changes based on cross-tissue proteomic profilling

ABSTRACT: The project aims to investigate the molecular mechanisms of aging by analyzing protein expression and modifications across various tissues in multiple organisms. Using advanced mass spectrometry, the project will collect and compare proteomic profiles from different organs at various ages. By identifying unique and shared aging-related biomarkers and pathways, the project seeks to enhance our understanding of the aging process and its impact on health. Ultimately, this research may pave the way for developing targeted therapies to improve healthspan and combat age-related diseases.

ORGANISM(S): Mus Musculus

SUBMITTER: Jun Zheng

PROVIDER: PXD061948 | iProX | Tue Mar 18 00:00:00 GMT 2025

REPOSITORIES: iProX

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Publications

Integrative cross-tissue analysis unveils complement-immunoglobulin augmentation and dysbiosis-related fatty acid metabolic remodeling during mammalian aging.

Zhang Feng F Li Rong R Liu Yasong Y Liang Jinliang J Gong Yihang Y Xiao Cuicui C Cai Jianye J Wang Tingting T You Qiang Q Zhang Jiebin J Chen Haitian H Xiao Jiaqi J Zhang Yingcai Y Yang Yang Y Li Hua H Yao Jia J Zhang Qi Q Zheng Jun J

iMeta 20250412 3

Aging-related decline and adaptation are complex, multifaceted processes that affect various tissues and increase risk of chronic diseases. To characterize key changes in cross-tissue aging, we performed comprehensive proteomic and metabolomic analyses across 21 solid tissues and plasma samples, alongside shotgun metagenomic profiling of fecal microbial communities in young and aged mice. Our findings revealed widespread aging-rewired chronic inflammation, characterized by complement system acti ...[more]

PMID: 40469517

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Project description:There has been a great deal of interest in identifying potential biomarkers of aging (Butler et al. 2004). Biomarkers of aging would be useful to predict potential vulnerabilities in an individual that may arise well before they are chronologically expected, due to idiosyncratic aging rates that occur between individuals. Prior attempts to identify biomarkers of aging have often relied on the comparisons of long-lived animals to a wild-type control (Dhahbi et al. 2004). However, the effect of interventions in model systems that prolong lifespan (such as single gene mutations, or caloric restriction) can sometimes be difficult to interpret due to the manipulation itself having multiple unforeseen consequences on physiology, unrelated to aging itself (Gems et al. 2002; Partridge & Gems 2006). The search for predictive biomarkers of aging therefore is problematic, and the identification of metrics that can be used to predict either physiological or chronological age would be of great value (Butler et al. 2004). One methodology which has been used to identify biomarkers for numerous pathologies is gene expression profiling. Here, we report whole-genome expression profiles of individual wild-type Caenorhabditis elegans covering the entire wild-type nematode life span. Individual nematodes were scored for either age-related behavioral phenotypes, or survival, and then subsequently associated with their respective gene expression profiles. This facilitated the identification of transcriptional profiles that were highly associated with either physiological or chronological age. Overall, our approach serves as a paradigm for identifying potential biomarkers of aging in higher organisms that can be repeatedly sampled throughout their lifespan. The full normalized data set with expression values for all genes of all individual worms at all ages (104 worms/arrays) is available as a 28Mb download as a supplementary file on this page (GSE12290.txt). Keywords: time couse Time course of aging in C. elegans. 7 ages were assayed, with a minimum of 9 biological replicates per timepoint, and as many as 17 biological replicates. All ages were compared to an independent 4 day old (young) pooled control.

Project description:Aims: Sarcopenia is the degenerative loss of skeletal muscle mass and function at high age, which affects 5-13% of people aged 60-70 years. Although a number of factors have been linked to sarcopenia, it remains unclear what determines its emergence in some but not all individuals and there are no medical treatments available. Mice and rats are widely used as model organisms to identify factors predisposing to sarcopenia, but the extent to which age-related molecular changes in wild-type mice and rats recapitulate those occurring in humans is not known. The aim of this project was to define a conserved set of regulators of aging-related reduction in muscle function that could be targeted by future therapies. Methods: We comparatively analyzed phenotypic parameters as well as the transcriptomes of the Gastrocnemius muscle from mice, rats and humans of a wide range of ages. We further inferred computationally the transcription regulators that likely underlie the molecular changes associated with aging-related loss in muscle functionality. Results: The analysis showed that the biological age of rodents that muscle mass is a better indicator of muscle functionality than the chronological age. Investigating the molecular changes associated with the aging-related loss of muscle mass, we discovered changes in gene expression that are shared between the studied species at the level of molecular pathways rather than at the level of individual genes. Beyond the known involvement of inflammation and mitochondrial function in aging, we found that the transcription regulators SPIB, ESRRB and YY1/YY2 consistently underlie aging-related molecular changes across the studied species. Conclusions: Rodents recapitulate well the molecular changes observed in human sarcopenia, but the conservation is stronger at the molecular pathway level than at the level of individual genes. Phenotypic parameters such as the muscle mass should be taken into account in stratifying samples for analyzing aging-related processes, as the chronological age is a poorer indicator of organ functionality. The shared regulators of aging-related muscle loss that we identified here can be studied further in rodent models of sarcopenia toward defining new targets for therapy in humans.

Dataset Information

Deciphering aging-related changes based on cross-tissue proteomic profilling

Publications

Integrative cross-tissue analysis unveils complement-immunoglobulin augmentation and dysbiosis-related fatty acid metabolic remodeling during mammalian aging.

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