ArticlePLoS biology2010
Widespread protein aggregation as an inherent part of aging in C. elegans.
Article in PLoS biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 371 papers, 2 of them syntheses that pooled it.
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
371 citing papers in PubMed, 2 syntheses or guidelines pooled it, 644 citations in OpenAlex.
- Meta-analysis of extracellular vesicles-associated protein abundance and aggregation during aging and disease in C. elegans.Biogerontology · 2025Pooled it
- A comparative meta-analysis of membraneless organelle-associated proteins with age related proteome of C. elegans.Cell stress & chaperones · 2022Pooled it
- Coordinated control of proteasome subunit gene expression promotes stress resistance, proteostasis, and longevity.GeroScience · 2026Article
- A neuronal GPCR modifies neuropeptide signaling to suppress proteostasis in distal tissues.Science advances · 2026Article
- Caenorhabditis elegans small heat-shock protein HSP-12.6 has a highly specialized protective function towards muscle thick filaments in vivo.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Article
- Combating ageing beyond the cell: Emerging roles of extracellular proteostasis.The FEBS journal · 2026Review
- Elevated levels of Ube2g1 in hematopoietic stem cells lead to segmental aging of the hematopoietic system.Haematologica · 2026Article
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Ultrasound-assisted extraction of bioactive phenolic compounds from walnut green husk: Phytochemical characterization and multi-endpointFood chemistry: X · 2026Article
- Insulin Signaling Functions as a Topological Switch That Couples Aging and Heat Stress Responsiveness.bioRxiv : the preprint server for biology · 2026Article
- Ago1 is required for the regulation of mitochondrial translation under heat stress in Schizosaccharomyces pombe.The Journal of biological chemistry · 2026Article
- Proteasome Dysfunction and Aggregation-Prone Proteins in Neurodegenerative Diseases: From Mechanisms to Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Nascent protein retention at polysomes reduces kinetic barriers to self-assembly.bioRxiv : the preprint server for biology · 2026Article
- Mitochondrial respiration modulates Hsf1 activation and the heat shock response.bioRxiv : the preprint server for biology · 2026Article
- Shifts in protein aggregate stability define proteostasis decline in the aging human brain.bioRxiv : the preprint server for biology · 2026Article
- Ribosome Molecular Aging Shapes Translation Dynamics.bioRxiv : the preprint server for biology · 2026Article
- Spatial protein expression patterns across pathologically-associated fibers revealed molecular specialization in inclusion body myositis.Cell communication and signaling : CCS · 2026Article
- Article
- Silencing lipid catabolism determines longevity in response to fasting.Nature communications · 2026Article
- Proteostasis breakdown and aggregate diversity in aging and neurodegenerative disease.Frontiers in aging neuroscience · 2026Review
311 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant protein aggregation is a hallmark of many age-related diseases, yet little is known about whether proteins aggregate with age in a non-disease setting. Using a systematic proteomics approach, we identified several hundred proteins that become more insoluble with age in the multicellular organism Caenorhabditis elegans. These proteins are predicted to be significantly enriched in beta-sheets, which promote disease protein aggregation. Strikingly, these insoluble proteins are highly over-represented in aggregates found in human neurodegeneration. We examined several of these proteins in vivo and confirmed their propensity to aggregate with age. Different proteins aggregated in different tissues and cellular compartments. Protein insolubility and aggregation were significantly delayed or even halted by reduced insulin/IGF-1-signaling, which also slows aging. We found a significant overlap between proteins that become insoluble and proteins that influence lifespan and/or polyglutamine-repeat aggregation. Moreover, overexpressing one aggregating protein enhanced polyglutamine-repeat pathology. Together our findings indicate that widespread protein insolubility and aggregation is an inherent part of aging and that it may influence both lifespan and neurodegenerative disease.
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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.