ArticleAging cell2022
S-adenosyl-L-homocysteine extends lifespan through methionine restriction effects.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- The AHCY-adenosine complex rewires mRNA methylation to enhance fatty acid biosynthesis and tumorigenesis.Cell research · 2026Article
- NSUN2-mediated HCV RNA m5C Methylation Facilitates Viral RNA Stability and Replication.Genomics, proteomics & bioinformatics · 2025Article
- Glibenclamide targets MDH2 to relieve aging phenotypes through metabolism-regulated epigenetic modification.Signal transduction and targeted therapy · 2025Article
- Diet-Modifiable Redox Alterations in Ageing and Cancer.Sub-cellular biochemistry · 2024Review
- Article
- The role of nutrition and oxidative stress as aging factors inJournal of clinical biochemistry and nutrition · 2023Article
- Modulation of DNA methylation by one-carbon metabolism: a milestone for healthy aging.Nutrition research and practice · 2023Review
- A set of common buccal CpGs that predict epigenetic age and associate with lifespan-regulating genes.iScience · 2022Article
- Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
Abstract
Methionine restriction (MetR) can extend lifespan and delay the onset of aging-associated pathologies in most model organisms. Previously, we showed that supplementation with the metabolite S-adenosyl-L-homocysteine (SAH) extends lifespan and activates the energy sensor AMP-activated protein kinase (AMPK) in the budding yeast Saccharomyces cerevisiae. However, the mechanism involved and whether SAH can extend metazoan lifespan have remained unknown. Here, we show that SAH supplementation reduces Met levels and recapitulates many physiological and molecular effects of MetR. In yeast, SAH supplementation leads to inhibition of the target of rapamycin complex 1 (TORC1) and activation of autophagy. Furthermore, in Caenorhabditis elegans SAH treatment extends lifespan by activating AMPK and providing benefits of MetR. Therefore, we propose that SAH can be used as an intervention to lower intracellular Met and confer benefits of MetR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.