ReviewDisease models & mechanisms2014
Caenorhabditis elegans as a model system for studying non-cell-autonomous mechanisms in protein-misfolding diseases.
Review in Disease models & mechanisms, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 61 citations in OpenAlex.
- Neuronal expression of bromodomain proteins alters neuronal health and peripheral protein homeostasis to promote longevity.Genes & development · 2026Article
- Modulation of host proteostasis by Prevotella corporis via induction of the heat shock response.Cell stress & chaperones · 2026Article
- Novel strategies for targeting tau oligomers in neurodegenerative diseases.Journal of neurology · 2025Review
- Loss of age-accumulatedFrontiers in aging neuroscience · 2025Article
- Hetero-oligomerization of TDP-43 carboxy-terminal fragments with cellular proteins contributes to proteotoxicity.Communications biology · 2024Article
- Probiotics for Neurodegenerative Diseases: A Systemic Review.Microorganisms · 2023Review
- C. elegans detects toxicity of traumatic brain injury generated tau.Neurobiology of disease · 2021Article
- Colonization of the Caenorhabditis elegans gut with human enteric bacterial pathogens leads to proteostasis disruption that is rescued by butyrate.PLoS pathogens · 2021Article
- HSF-1 displays nuclear stress body formation in multiple tissues in Caenorhabditis elegans upon stress and following the transition to adulthood.Cell stress & chaperones · 2021Article
- Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.Progress in molecular and subcellular biology · 2021Article
- Review
- Chemical Penetration Enhancers Increase Hydrogen Peroxide Uptake inJournal of proteome research · 2020Article
- Article
- Reducing INS-IGF1 signaling protects against non-cell autonomous vesicle rupture caused by SNCA spreading.Autophagy · 2020Article
- Article
- Amyotrophic Lateral Sclerosis: Proteins, Proteostasis, Prions, and Promises.Frontiers in cellular neuroscience · 2020Article
- Article
- Illuminating Biological Interactions with in Vivo Protein Footprinting.Analytical chemistry · 2019Article
- Contributions of Animal Models to the Mechanisms and Therapies of Transthyretin Amyloidosis.Frontiers in physiology · 2019Review
- Application ofPreventive nutrition and food science · 2018Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Caenorhabditis elegans has a number of distinct advantages that are useful for understanding the basis for cellular and organismal dysfunction underlying age-associated diseases of protein misfolding. Although protein aggregation, a key feature of human neurodegenerative diseases, has been typically explored in vivo at the single-cell level using cells in culture, there is now increasing evidence that proteotoxicity has a non-cell-autonomous component and is communicated between cells and tissues in a multicellular organism. These discoveries have opened up new avenues for the use of C. elegans as an ideal animal model system to study non-cell-autonomous proteotoxicity, prion-like propagation of aggregation-prone proteins, and the organismal regulation of stress responses and proteostasis. This Review focuses on recent evidence that C. elegans has mechanisms to transmit certain classes of toxic proteins between tissues and a complex stress response that integrates and coordinates signals from single cells and tissues across the organism. These findings emphasize the potential of C. elegans to provide insights into non-cell-autonomous proteotoxic mechanisms underlying age-related protein-misfolding diseases.
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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.