ReviewFree radical biology & medicine2015
Collaboration between mitochondria and the nucleus is key to long life in Caenorhabditis elegans.
Review in Free radical biology & medicine, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed.
- Mitochondrial pathways in human health and aging.Mitochondrion · 2020Review
- Mitochondria-cytosol-nucleus crosstalk: learning from Saccharomyces cerevisiae.FEMS yeast research · 2018Review
- Genetic inhibition of an ATP synthase subunit extends lifespan in C. elegans.Scientific reports · 2018Article
- Article
- Article
- Effects of Sex, Strain, and Energy Intake on Hallmarks of Aging in Mice.Cell metabolism · 2016Article
- The Aging Epigenome.Molecular cell · 2016Review
- The metabolic regulation of aging.Nature medicine · 2015Review
- Dietary restriction, mitochondrial function and aging: from yeast to humans.Biochimica et biophysica acta · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Recent findings in diverse organisms strongly support a conserved role for mitochondrial electron transport chain dysfunction in longevity modulation, but the underlying mechanisms are not well understood. One way cells cope with mitochondrial dysfunction is through a retrograde transcriptional reprogramming response. In this review, we primarily focus on the work that has been performed in Caenorhabditis elegans to elucidate these mechanisms. We describe several transcription factors that participate in mitochondria-to-nucleus signaling and discuss how they mediate the relationship between mitochondrial dysfunction and life span.
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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.