ArticleCell2016
Neuroendocrine Coordination of Mitochondrial Stress Signaling and Proteostasis.
Article in Cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 150 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
150 citing papers in PubMed, 247 citations in OpenAlex.
- Ginsenoside Rg3 Promotes Healthy Aging Through Phosphoinositide-Associated Lysosomal Regulation in Caenorhabditis elegans.Aging cell · 2026Article
- Regulation of cellular proteostasis via mitochondrial protein import.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2026Review
- Balancing mitochondrial health through inter-tissue neurotransmitter signaling.Neural regeneration research · 2026Article
- Heat stress reveals bidirectional cross talk between the heat shock response and UPRER in C. elegans.G3 (Bethesda, Md.) · 2026Article
- The mitochondrial unfolded protein response in human microglia disrupts neuronal-glial communication and promotes senescence.Nature neuroscience · 2026Article
- FUBL-3/FUBP1 mediates mitochondrial stress-induced chromatin remodeling and longevity.Science advances · 2026Article
- A Forward Genetic Screen inbioRxiv : the preprint server for biology · 2026Article
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Phosphorylated ubiquitin is a secondary messenger and an epigenetic mark mediating mitochondria to nucleus signaling.bioRxiv : the preprint server for biology · 2026Article
- Eyeless light sensing promotes thermotolerance.Cell research · 2026Article
- Gas-sensing neurons prime mitochondrial fitness to offset metabolic stress.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Isoflurane aggravates pre-existing proteotoxicity in adult nematodes by suppressing mitochondrial fitness.Scientific reports · 2026Article
- Adaptive inter-tissue proteostasis networks in aging and neurodegeneration.Bioscience reports · 2026Review
- Multilayered regulation of longevity in Caenorhabditis elegans.Molecules and cells · 2026Review
- Mitochondrial unfolded protein response as a central stress-integration hub: mechanisms and implications in disease contexts.Burns & trauma · 2026Review
- The microRNA miR-71 suppresses maladaptive UPRNature communications · 2025Article
- Article
- Soma to neuron communication links stress adaptation to stress avoidance behavior.bioRxiv : the preprint server for biology · 2025Article
- Heat shock proteins function as signaling molecules to mediate neuron-glia communication in C. elegans during aging.Nature neuroscience · 2025Article
- Cross-comparison of strains used for mitochondrial imaging inLife science alliance · 2025Article
90 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
During neurodegenerative disease, the toxic accumulation of aggregates and misfolded proteins is often accompanied with widespread changes in peripheral metabolism, even in cells in which the aggregating protein is not present. The mechanism by which the central nervous system elicits a distal reaction to proteotoxic stress remains unknown. We hypothesized that the endocrine communication of neuronal stress plays a causative role in the changes in mitochondrial homeostasis associated with proteotoxic disease states. We find that an aggregation-prone protein expressed in the neurons of C. elegans binds to mitochondria, eliciting a global induction of a mitochondrial-specific unfolded protein response (UPR(mt)), affecting whole-animal physiology. Importantly, dense core vesicle release and secretion of the neurotransmitter serotonin is required for the signal's propagation. Collectively, these data suggest the commandeering of a nutrient sensing network to allow for cell-to-cell communication between mitochondria in response to protein folding stress in the nervous system.
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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.