ArticleAging2010
Chemical genetic screen identifies lithocholic acid as an anti-aging compound that extends yeast chronological life span in a TOR-independent manner, by modulating housekeeping longevity assurance processes.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
75 citing papers in PubMed, 117 citations in OpenAlex.
- The protein phosphatase 6 subunit SAPS3 modulates lifespan by regulating metabolism.Science advances · 2025Article
- Article
- Article
- The phenomenon of anhydrobiosis-structural and functional changes in yeast cells.Applied microbiology and biotechnology · 2025Review
- Article
- Review
- Diverse geroprotectors differently affect a mechanism linking cellular aging to cellular quiescence in budding yeast.Oncotarget · 2022Article
- The Effect of Lithocholic Acid on the Gut-Liver Axis.Frontiers in pharmacology · 2022Review
- Caloric restriction causes a distinct reorganization of the lipidome in quiescent and non-quiescent cells of budding yeast.Oncotarget · 2021Article
- Article
- Article
- The road ahead for health and lifespan interventions.Ageing research reviews · 2020Review
- Characterization of survival and stress resistance in S. cerevisiae mutants affected in peroxisome inheritance and proliferation, Δinp1 and Δpex11.Folia microbiologica · 2020Article
- Mechanisms by which PE21, an extract from the white willowOncotarget · 2019Article
- Article
- Article
- Mechanisms through which lithocholic acid delays yeast chronological aging under caloric restriction conditions.Oncotarget · 2018Article
- Yeast as a tool to identify anti-aging compounds.FEMS yeast research · 2018Review
- Methionine Restriction Extends Lifespan in Progeroid Mice and Alters Lipid and Bile Acid Metabolism.Cell reports · 2018Article
- Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Commented on by
- Commented on by
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
Abstract
In chronologically aging yeast, longevity can be extended by administering a caloric restriction (CR) diet or some small molecules. These life-extending interventions target the adaptable target of rapamycin (TOR) and cAMP/protein kinase A (cAMP/PKA) signaling pathways that are under the stringent control of calorie availability. We designed a chemical genetic screen for small molecules that increase the chronological life span of yeast under CR by targeting lipid metabolism and modulating housekeeping longevity pathways that regulate longevity irrespective of the number of available calories. Our screen identifies lithocholic acid (LCA) as one of such molecules. We reveal two mechanisms underlying the life-extending effect of LCA in chronologically aging yeast. One mechanism operates in a calorie availability-independent fashion and involves the LCA-governed modulation of housekeeping longevity assurance pathways that do not overlap with the adaptable TOR and cAMP/PKA pathways. The other mechanism extends yeast longevity under non-CR conditions and consists in LCA-driven unmasking of the previously unknown anti-aging potential of PKA. We provide evidence that LCA modulates housekeeping longevity assurance pathways by suppressing lipid-induced necrosis, attenuating mitochondrial fragmentation, altering oxidation-reduction processes in mitochondria, enhancing resistance to oxidative and thermal stresses, suppressing mitochondria-controlled apoptosis, and enhancing stability of nuclear and mitochondrial DNA.
Indexed as
Identifiers
What OpenQuestion holds
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.