ArticleCell2011
The cell-non-autonomous nature of electron transport chain-mediated longevity.
Article in Cell, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 667 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.
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Who cites it
667 citing papers in PubMed.
- Dichloroacetate Improves Animal Survival, Growth, Neuromuscular Activity, Mitochondrial Stress and Physiology, and Elevated Lactate in C. elegans pdha-1 and dld-1 RNAi Models of Pyruvate Dehydrogenase Complex Deficiency (PDCD).Journal of inherited metabolic disease · 2026Article
- Form and function of actin impacts actin health and aging.iScience · 2026Article
- Divergent Retrograde Signaling Pathways Coordinate Longevity and Metformin Responses in Complex I and Complex IV DeficientbioRxiv : the preprint server for biology · 2026Article
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- Neuronal expression of bromodomain proteins alters neuronal health and peripheral protein homeostasis to promote longevity.Genes & development · 2026Article
- Mitochondrial stress activates ELT-2-dependent lysosomal proteostasis to extend lifespan inScience advances · 2026Article
- The mitochondrial unfolded protein response in human microglia disrupts neuronal-glial communication and promotes senescence.Nature neuroscience · 2026Article
- A Purified Lycii Fructus Polysaccharide Fraction Extends Healthspan inAntioxidants (Basel, Switzerland) · 2026Article
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Proteostasis Rebalancing by LET-607 Deficiency Promotes Longevity.Aging cell · 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
- Tuning the Fire: Context-Dependent Mitochondrial ROS Signaling, Mitohormesis, and Redox-Modulating Interventions.Biomolecules · 2026Review
- Nuclear-Mitochondria Crosstalk in Senescent Adipose-Derived Stem Cells.Smart medicine · 2026Review
- Unfolding Resilience: Molecular Integration of the Integrated Stress Response and Mitochondrial UPR in Skeletal Muscle Homeostasis.Muscles (Basel, Switzerland) · 2026Review
- A Stress-Responsive Nuclear Factor, GLDI-8, Mediates Mitochondrial Stress Responses to ETC Dysfunction.International journal of molecular sciences · 2026Article
- Structure-guided identification of small molecules potentially able to modulate GDF15 activity.Scientific reports · 2026Article
- MAK-2 Kinase Is Required for Extended Longevity and Enhanced Stress Resistance Resulting From Mild Impairment of Mitochondrial Function in isp-1 Mutants.Aging cell · 2026Article
- Organellar insights in ageing and longevity.Nature cell biology · 2026Review
- Adulthood depletion of Integrator extends lifespan and healthspan via defective pre-mRNA processing.bioRxiv : the preprint server for biology · 2026Article
607 more citing papers are in PubMed but not listed here.
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Authors and funding
3 authors.
Funding
Abstract
The life span of C. elegans can be increased via reduced function of the mitochondria; however, the extent to which mitochondrial alteration in a single, distinct tissue may influence aging in the whole organism remains unknown. We addressed this question by asking whether manipulations to ETC function can modulate aging in a cell-non-autonomous fashion. We report that the alteration of mitochondrial function in key tissues is essential for establishing and maintaining a prolongevity cue. We find that regulators of mitochondrial stress responses are essential and specific genetic requirements for the electron transport chain (ETC) longevity pathway. Strikingly, we find that mitochondrial perturbation in one tissue is perceived and acted upon by the mitochondrial stress response pathway in a distal tissue. These results suggest that mitochondria may establish and perpetuate the rate of aging for the whole organism independent of cell-autonomous functions.
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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.