ArticlePloS one2016
The Mitochondrial Unfolded Protein Response Protects against Anoxia in Caenorhabditis elegans.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial dynamics and quality control regulate proteostasis in neuronal ischemia-reperfusion.Autophagy · 2025Article
- Mild activation of the mitochondrial unfolded protein response increases lifespan without increasing resistance to stress.Open biology · 2025Article
- Mitochondrial Unfolded Protein Response (mtUPR) and Diseases.Current medicinal chemistry · 2025Review
- Transcutaneous Auricular Vagus Nerve Stimulation Ameliorates Preeclampsia-Induced Apoptosis of Placental Trophoblastic Cells Via Inhibiting the Mitochondrial Unfolded Protein Response.Neuroscience bulletin · 2024Article
- CTRP3 alleviates mitochondrial dysfunction and oxidative stress injury in pathological cardiac hypertrophy by activating UPRmt via the SIRT1/ATF5 axis.Cell death discovery · 2024Article
- UNC-49 is a redox-sensitive GABAScience advances · 2023Article
- Mitochondrial Factors in the Cell Nucleus.International journal of molecular sciences · 2023Review
- Hypoxia-induced mitochondrial stress granules.Cell death & disease · 2023Article
- Mitochondrial Protein Homeostasis and Cardiomyopathy.International journal of molecular sciences · 2022Review
- Activation of mitochondrial unfolded protein response protects against multiple exogenous stressors.Life science alliance · 2021Article
- FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.Autophagy · 2021Article
- Identification of enzymes that have helminth-specific active sites and are required for Rhodoquinone-dependent metabolism as targets for new anthelmintics.PLoS neglected tropical diseases · 2021Article
- Roles of mitochondrial unfolded protein response in mammalian stem cells.World journal of stem cells · 2021Review
- Effect of the mitochondrial unfolded protein response on hypoxic death and mitochondrial protein aggregation.Cell death & disease · 2021Article
- Preconditioning of Caenorhabditis elegans to anoxic insult by inactivation of cholinergic, GABAergic and muscle activity.Genes, brain, and behavior · 2021Article
- Decreased Mitochondrial Membrane Potential Activates the Mitochondrial Unfolded Protein Response.microPublication biology · 2021Article
- Neuronal AMPK coordinates mitochondrial energy sensing and hypoxia resistance in C. elegans.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- A T231E Mutant that Mimics Pathologic Phosphorylation of Tau in Alzheimer's disease Causes Activation of the Mitochondrial Unfolded Protein Response inmicroPublication biology · 2020Article
- Optogenetic control of mitochondrial protonmotive force to impact cellular stress resistance.EMBO reports · 2020Article
- Cardioprotection by the mitochondrial unfolded protein response requires ATF5.American journal of physiology. Heart and circulatory physiology · 2019Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The mitochondrial unfolded protein response (UPRmt) is a surveillance pathway that defends proteostasis in the "powerhouse" of the cell. Activation of the UPRmt protects against stresses imposed by reactive oxygen species, respiratory chain deficits, and pathologic bacteria. Consistent with the UPRmt's role in adaption, we found that either its pharmacological or genetic activation by ethidium bromide (EtBr) or RNAi of the mitochondrial AAA-protease spg-7 was sufficient to reduce death in an anoxia-based Caenorhabditis elegans model of ischemia-reperfusion injury. The UPRmt-specific transcription factor atfs-1 was necessary for protection and atfs-1 gain-of-function (gf) mutants were endogenously protected from both death and dysfunction. Neurons exhibited less axonal degeneration following non-lethal anoxia-reperfusion (A-R) when the UPRmt was pre-activated, and consistent with the concept of mitochondrial stress leading to cell non-autonomous (ie. "remote") effects, we found that restricted activation of the UPRmt in neurons decreased A-R death. However, expression of the atfs-1(gf) mutant in neurons, which resulted in a robust activation of a neuronal UPRmt, did not upregulate the UPRmt in distal tissues, nor did it protect the worms from A-R toxicity. These findings suggest that remote signaling requires additional component(s) acting downstream of de facto mitochondrial stress.
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Registered trials
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