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Metabolic modeling reveals the aging-associated decline of host–microbiome metabolic interactions in mice

ABSTRACT: Metabolic modeling reveals the aging-associated decline of host–microbiome metabolic interactions in mice

PROVIDER: PRJNA1090973 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR28424100_1.fastq.gz	Fastqsanger.gz
	SRR28424100_2.fastq.gz	Fastqsanger.gz
	SRR28424200_1.fastq.gz	Fastqsanger.gz
	SRR28424200_2.fastq.gz	Fastqsanger.gz
	SRR28424101_1.fastq.gz	Fastqsanger.gz

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Metabolic modeling reveals the aging-associated decline of host-microbiome metabolic interactions in mice

Project description:Metabolic modeling reveals the aging-associated decline of host-microbiome metabolic interactions in mice

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Metabolic modeling reveals the aging-associated decline of host–microbiome metabolic interactions in mice

Project description:Aging is the predominant cause of morbidity and mortality in industrialized countries. The specific molecular mechanisms that drive aging are poorly understood, especially the contribution of the microbiota in these processes. Here, we combined multi-omics with metabolic modeling in mice to comprehensively characterize host–microbiome interactions and how they are affected by aging. Our findings reveal a complex dependency of host metabolism on microbial functions, including previously known as well as novel interactions. We observed a pronounced reduction in metabolic activity within the aging microbiome, which we attribute to reduced beneficial interactions in the microbial community and a reduction in the metabolic output of the microbiome. These microbial changes coincided with a corresponding downregulation of key host pathways predicted by our model that are crucial for maintaining intestinal barrier function, cellular replication, and homeostasis. Our results elucidate potential microbiome–host interactions that may influence host aging processes, focusing on microbial nucleotide metabolism as a pivotal factor in aging dynamics.

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Project description:The decline of endothelial autophagy is closely related to vascular senescence and disease, although the molecular mechanisms connecting these outcomes in vascular endothelial cells (VECs) remain unclear. Here, we identify a crucial role for CD44, a multifunctional adhesion molecule, in controlling autophagy and aging in VECs. The CD44 intercellular domain (CD44ICD) negatively regulates autophagy by reducing PIK3R4 and PIK3C3 levels and disrupting STAT3-dependent PtdIns3K complexes. CD44 and its homologue clec-31 are increased in aging vascular endothelium and Caenorhabditis elegans, respectively, suggesting that an age-dependent increase in CD44 induces autophagy decline and aging phenotypes. Accordingly, CD44 knockdown ameliorates age-associated phenotypes in VECs. The endothelium-specific CD44ICD knock-in mouse is shorter-lived, with VECs exhibiting obvious premature aging characteristics associated with decreased basal autophagy. Autophagy activation suppresses the premature aging of human and mouse VECs overexpressing CD44ICD, function conserved in the CD44 homologue clec-31 in C. elegans. Our work describes a mechanism coordinated by CD44 function bridging autophagy decline and aging.

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