ArticlePLoS genetics2020
Autophagy compensates for defects in mitochondrial dynamics.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Transcriptomic analysis of mitohormesis associated with lifespan extension in Caenorhabditis elegans.GeroScience · 2026Article
- Mitochondria-Targeted Au@Carbon Dot Nanoprobes for SERS Analysis of Drug-Induced Mitophagy.Chemical & biomedical imaging · 2026Article
- Mapping the global research landscape of mitophagy in Parkinson's disease: a bibliometric and visualization analysis.Hereditas · 2025Article
- Article
- The Juvenile Parkinson's Disease Mutation C212Y Impairs Mitochondrial Homeostasis in a Caenorhabditis elegans Model.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Peripheral immune cell response to stimulation stratifies Parkinson's disease progression from prodromal to clinical stages.Communications biology · 2025Article
- VPS13D mutations affect mitochondrial homeostasis and locomotion in Caenorhabditis elegans.G3 (Bethesda, Md.) · 2025Article
- Phosphorylated glycosphingolipids are commonly detected in Caenorhabditis elegans lipidomes.Metabolomics : Official journal of the Metabolomic Society · 2025Article
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
- ULP-2 SUMO protease regulates UPRFree radical biology & medicine · 2024Article
- Mitochondrial recovery by the UPRSeminars in cell & developmental biology · 2024Review
- A p-Tyr42 RhoA Inhibitor Promotes the Regeneration of Human Corneal Endothelial Cells by Ameliorating Cellular Senescence.Antioxidants (Basel, Switzerland) · 2023Article
- Role of UPRFrontiers in cellular and infection microbiology · 2023Review
- Article
- Hijacking Cellular Stress Responses to Promote Lifespan.Frontiers in aging · 2022Review
- Dynamic observation of 5-fluorouracil-induced myocardial injury and mitochondrial autophagy in aging rats.Experimental and therapeutic medicine · 2021Article
- FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.Autophagy · 2021Article
- Cross-species screening platforms identify EPS-8 as a critical link for mitochondrial stress and actin stabilization.Science advances · 2021Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Compromising mitochondrial fusion or fission disrupts cellular homeostasis; however, the underlying mechanism(s) are not fully understood. The loss of C. elegans fzo-1MFN results in mitochondrial fragmentation, decreased mitochondrial membrane potential and the induction of the mitochondrial unfolded protein response (UPRmt). We performed a genome-wide RNAi screen for genes that when knocked-down suppress fzo-1MFN(lf)-induced UPRmt. Of the 299 genes identified, 143 encode negative regulators of autophagy, many of which have previously not been implicated in this cellular quality control mechanism. We present evidence that increased autophagic flux suppresses fzo-1MFN(lf)-induced UPRmt by increasing mitochondrial membrane potential rather than restoring mitochondrial morphology. Furthermore, we demonstrate that increased autophagic flux also suppresses UPRmt induction in response to a block in mitochondrial fission, but not in response to the loss of spg-7AFG3L2, which encodes a mitochondrial metalloprotease. Finally, we found that blocking mitochondrial fusion or fission leads to increased levels of certain types of triacylglycerols and that this is at least partially reverted by the induction of autophagy. We propose that the breakdown of these triacylglycerols through autophagy leads to elevated metabolic activity, thereby increasing mitochondrial membrane potential and restoring mitochondrial and cellular homeostasis.
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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.