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Drug synergy slows ageing and improves healthspan through IGF and SREBP lipid signaling

ABSTRACT: Drug synergy slows ageing and improves healthspan through IGF and SREBP lipid signaling

PROVIDER: PRJNA423001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6388520_1.fastq.gz	Fastqsanger.gz
	SRR6388520_2.fastq.gz	Fastqsanger.gz
	SRR6388530_1.fastq.gz	Fastqsanger.gz
	SRR6388530_2.fastq.gz	Fastqsanger.gz
	SRR6388540_1.fastq.gz	Fastqsanger.gz

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Drug synergy slows ageing and improves healthspan through IGF and SREBP lipid signaling

Project description:Pharmacological interventions directly modulating ageing would extend human healthspan, resulting in dramatic medical and economic benefits. Such interventions should be efficacious in adults and ideally repurpose drugs known to be safe. Here we show that dramatic lifespan extension can be achieved by targeting multiple, evolutionarily conserved ageing pathways using drugs already used in humans. Using this approach in C. elegans, we were able to slow ageing, improve healthspan and minimize trade-offs. We show that daf-2, daf-7 and sbp-1 (mammalian SREBP-1c) interact upstream of changes in lipid metabolism, resulting in increased monounsaturated fatty acid content and lifespan extension. For one combination, we observed evolutionary conservation in fruit flies. To the best of our knowledge, this is the largest lifespan effect ever reported for any adult-onset drug treatment in C. elegans. Drug repurposing approaches, by leveraging drugs already approved for humans, could lead to rapid translation of experimental results to clinical applications.

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Caenorhabditis elegans strain:N2 and eat-2

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Project description:The role of ellagic acid (EA), a natural antioxidant, in regulating anti-aging and its underlying mechanisms remains unclear. In this study, we investigated the anti-aging effects and molecular mechanisms of EA in Caenorhabditis elegans (C. elegans). Our results demonstrate that EA extends the lifespan of C. elegans, enhances motility, reduces lipofuscin accumulation, and improves overall healthspan. Additionally, EA reduces reactive oxygen species (ROS) accumulation in C. elegans under conditions of heat and oxidative stress. The insulin/IGF-1 signaling (IIS) pathway, a key regulator of longevity and stress resistance in C. elegans, was found to mediate EA's effects. EA treatment did not extend the lifespan of mutants defective in daf-2, daf-16, hsf-1, hlh-30, and skn-1, confirming that EA’s lifespan-extending effect operates through the IIS pathway. Furthermore, EA treatment increased the expression of stress response genes downstream of the IIS pathway. Based on RNA sequencing data, we further explored the molecular mechanisms and potential regulatory roles of EA in anti-aging.

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Ellagic Acid Enhances Longevity and Healthspan in Caenorhabditis elegans via Insulin/IGF-1 Signaling Pathway

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A torpor-like state in mice slows blood epigenetic aging and prolongs healthspan

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