ArticleNature aging2024
Early life changes in histone landscape protect against age-associated amyloid toxicities through HSF-1-dependent regulation of lipid metabolism.
Article in Nature aging, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 17 citations in OpenAlex.
- Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.The EMBO journal · 2026Article
- Article
- HSF-1 Regulates Autophagy to Govern Motor Function and Facilitate Toxic Protein Clearance in a C. elegans Model of Amyotrophic Lateral Sclerosis.Neuroscience bulletin · 2026Article
- Stress-associated High Production of Large Extracellular Vesicles in the Parent Generation is Not Inherited by microPublication biology · 2026Article
- HSF1 modulates lipid metabolism and ferroptosis in sarcopenia: a novel diagnostic biomarker and therapeutic target.Frontiers in molecular biosciences · 2026Article
- Dysregulated hippocampal fatty acid metabolism following intermittent hypoxemia-induced neonatal brain injury is rescued by treatment with acetate.Nature communications · 2025Article
- Lactate promotes longevity through redox-driven lipid remodeling inbioRxiv : the preprint server for biology · 2025Article
- HSF-1 promotes longevity through ubiquilin-1-dependent mitochondrial network remodelling.Nature communications · 2024Article
- Cellular oxidants and the proteostasis network: balance between activation and destruction.Trends in biochemical sciences · 2024Review
- Fundamentals of redox regulation in biology.Nature reviews. Molecular cell biology · 2024Review
- Histone deacetylase inhibition expands cellular proteostasis repertoires to enhance neuronal stress resilience.bioRxiv : the preprint server for biology · 2024Article
- Early-life stress triggers long-lasting organismal resilience and longevity via tetraspanin.Science advances · 2024Article
- Early exposure to a systemic stressor confers protection later in life.Nature aging · 2024Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
Transient events during development can exert long-lasting effects on organismal lifespan. Here we demonstrate that exposure of Caenorhabditis elegans to reactive oxygen species during development protects against amyloid-induced proteotoxicity later in life. We show that this protection is initiated by the inactivation of the redox-sensitive H3K4me3-depositing COMPASS complex and conferred by a substantial increase in the heat-shock-independent activity of heat shock factor 1 (HSF-1), a longevity factor known to act predominantly during C. elegans development. We show that depletion of HSF-1 leads to marked rearrangements of the organismal lipid landscape and a significant decrease in mitochondrial β-oxidation and that both lipid and metabolic changes contribute to the protective effects of HSF-1 against amyloid toxicity. Together, these findings link developmental changes in the histone landscape, HSF-1 activity and lipid metabolism to protection against age-associated amyloid toxicities later in life.
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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.