ArticleCell2013
XBP-1 is a cell-nonautonomous regulator of stress resistance and longevity.
Article in Cell, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 375 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
375 citing papers in PubMed, 607 citations in OpenAlex.
- Proteostasis of organelles in aging and disease.The FEBS journal · 2026Review
- Biogenesis of TNF-α-insights into proteostasis and inflammation.The FEBS journal · 2026Review
- Neuronal expression of bromodomain proteins alters neuronal health and peripheral protein homeostasis to promote longevity.Genes & development · 2026Article
- Heat stress reveals bidirectional cross talk between the heat shock response and UPRER in C. elegans.G3 (Bethesda, Md.) · 2026Article
- Sensory decline in aging and neurodegeneration: A mitochondrial perspective.Pharmacological research · 2026Review
- Developmental priming of adult proteostasis and longevity by NuA4 complex activity in early life.The EMBO journal · 2026Article
- Proteostasis Rebalancing by LET-607 Deficiency Promotes Longevity.Aging cell · 2026Article
- Suppression rather than activation of the integrated stress response (GCN2-ATF4) pathway extends lifespan in the fly.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Adaptive ER stress promotes mitochondrial remodelling and longevity through PERK-dependent MERCS assembly.Cell death and differentiation · 2026Article
- A neuropeptide regulates cell non-autonomous protein homeostasis.Cell reports · 2026Article
- Heat shock factor-1 alleviates ER-stress in Caenorhabditis elegans.Scientific reports · 2026Article
- Cycloneolitsol prolongs the lifespan of Caenorhabditis elegans by SEK-1/PMK-1/SKN-1 pathway and exerts anti-inflammatory effects by NF-κB pathway.Biogerontology · 2026Article
- Unlocking neuronal health: leveraging C. elegans for drug repurposing studies.Cell communication and signaling : CCS · 2026Review
- Adaptive inter-tissue proteostasis networks in aging and neurodegeneration.Bioscience reports · 2026Review
- Exploring non-autonomous protein homeostasis driven by glutamatergic neurons.microPublication biology · 2026Article
- X-Box Binding Protein 1 Regulates Osteogenesis of Periodontal Ligament Cells During Aging by Modulating P53 Signaling Pathway.Stem cells international · 2026Article
- Lessons in longevity from blood stem cells under protein stress.Trends in cell biology · 2026Review
- Reduction of calreticulin and ERp57 with age reveals the ER stress-related roles in cell viability and organismal lifespan regulation.Frontiers in aging · 2026Article
- Functionally diversified Caenorhabditis elegans BiP orthologs control body growth, reproduction, stress resistance, aging, and autophagy.Nature communications · 2025Article
315 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The ability to ensure proteostasis is critical for maintaining proper cell function and organismal viability but is mitigated by aging. We analyzed the role of the endoplasmic reticulum unfolded protein response (UPR(ER)) in aging of C. elegans and found that age-onset loss of ER proteostasis could be reversed by expression of a constitutively active form of XBP-1, XBP-1s. Neuronally derived XBP-1s was sufficient to rescue stress resistance, increase longevity, and activate the UPR(ER) in distal, non-neuronal cell types through a cell-nonautonomous mechanism. Loss of UPR(ER) signaling components in distal cells blocked cell-nonautonomous signaling from the nervous system, thereby blocking increased longevity of the entire animal. Reduction of small clear vesicle (SCV) release blocked nonautonomous signaling downstream of xbp-1s, suggesting that the release of neurotransmitters is required for this intertissue signaling event. Our findings point toward a secreted ER stress signal (SERSS) that promotes ER stress resistance and longevity.
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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.