ReviewRedox biology2014
Mitochondrial stress signaling in longevity: a new role for mitochondrial function in aging.
Review in Redox biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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
70 citing papers in PubMed, 128 citations in OpenAlex.
- Transcranial Photobiomodulation (tPBM) With 1,064-nm Laser to Improve Cerebral Metabolism of the Human Brain In Vivo.Lasers in surgery and medicine · 2020Trial
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- Nanosecond pulsed electric field applications rejuvenate aging endothelial cells by rescuing mitochondrial-to-nuclear retrograde communication.Regenerative therapy · 2025Article
- Mitochondria in oxidative stress, inflammation and aging: from mechanisms to therapeutic advances.Signal transduction and targeted therapy · 2025Review
- Integrated analysis of transcriptional and metabolic responses to mitochondrial stress.Cell reports methods · 2025Article
- Identifying ENO1 as a protein target of chlorogenic acid to inhibit cellular senescence and prevent skin photoaging in mice.Aging cell · 2025Article
- Actives from the Micro-Immunotherapy Medicine 2LMIREGJournal of inflammation research · 2024Article
- Bio-Hacking Better Health-Leveraging Metabolic Biochemistry to Maximise Healthspan.Antioxidants (Basel, Switzerland) · 2023Article
- Potential Active Marine Peptides as Anti-Aging Drugs or Drug Candidates.Marine drugs · 2023Review
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- Comparison betweenInternational journal of fertility & sterility · 2022Article
- An orchestrating role of mitochondria in the origin and development of post-traumatic stress disorder.Frontiers in physiology · 2022Review
- Mitochondrial stress response in drug-induced liver injury.Molecular biology reports · 2021Review
- Anterograde regulation of mitochondrial genes and FGF21 signaling by hepatic LSD1.JCI insight · 2021Article
- Chromatin remodeling due to degradation of citrate carrier impairs osteogenesis of aged mesenchymal stem cells.Nature aging · 2021Article
- Review
- Article
- Mitochondrial transplantation therapy inhibit carbon tetrachloride-induced liver injury through scavenging free radicals and protecting hepatocytes.Bioengineering & translational medicine · 2021Article
- Mechanisms and regulation of protein synthesis in mitochondria.Nature reviews. Molecular cell biology · 2021Review
10 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
2 authors at 2 institutions in 1 country.
Funding
Abstract
Mitochondria are principal regulators of cellular function and metabolism through production of ATP for energy homeostasis, maintenance of calcium homeostasis, regulation of apoptosis and fatty acid oxidation to provide acetyl CoA for fueling the electron transport chain. In addition, mitochondria play a key role in cell signaling through production of reactive oxygen species that modulate redox signaling. Recent findings support an additional mechanism for control of cellular and tissue function by mitochondria through complex mitochondrial-nuclear communication mechanisms and potentially through extracellular release of mitochondrial components that can act as signaling molecules. The activation of stress responses including mitophagy, mitochondrial number, fission and fusion events, and the mitochondrial unfolded protein response (UPR(MT)) requires mitochondrial-nuclear communication for the transcriptional activation of nuclear genes involved in mitochondrial quality control and metabolism. The induction of these signaling pathways is a shared feature in long-lived organisms spanning from yeast to mice. As a result, the role of mitochondrial stress signaling in longevity has been expansively studied. Current and exciting studies provide evidence that mitochondria can also signal among tissues to up-regulate cytoprotective activities to promote healthy aging. Alternatively, mitochondria release signals to modulate innate immunity and systemic inflammatory responses and could consequently promote inflammation during aging. In this review, established and emerging models of mitochondrial stress response pathways and their potential role in modulating longevity are discussed.
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Identifiers
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.