ArticleFly2016
Mitochondrial retrograde signaling in the Drosophila nervous system and beyond.
Article in Fly, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
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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
7 citing papers in PubMed, 12 citations in OpenAlex.
- A Drosophila model of mitochondrial disease phenotypic heterogeneity.Biology open · 2024Article
- Mind the Gap: Mitochondria and the Endoplasmic Reticulum in Neurodegenerative Diseases.Biomedicines · 2021Review
- Decoding the rosetta stone of mitonuclear communication.Pharmacological research · 2020Review
- Phenolic Acids-Rich Fractions fromMolecules (Basel, Switzerland) · 2020Article
- Mitochondrial retrograde signalling in neurological disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Review
- Ras-ERK-ETS inhibition alleviates neuronal mitochondrial dysfunction by reprogramming mitochondrial retrograde signaling.PLoS genetics · 2018Article
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 1 institution in 1 country.
Funding
Abstract
Mitochondrial dysfunction has been suggested to contribute to neurodegenerative diseases, including Alzheimer and Parkinson disease. Cells respond to changes in the functional state of mitochondria via retrograde signaling pathways from the mitochondria to the nucleus, but little is known about retrograde signaling in the nervous system. We have recently shown that inhibition of retrograde signaling reduces the impact of neuronal mitochondrial dysfunction. We performed a study designed to characterize the mitochondrial retrograde signaling pathway in the Drosophila nervous system. Using several different models we found that neuronal specific mitochondrial dysfunction results in defects in synapse development and neuronal function. Moreover, we identified the Drosophila hypoxia inducible factor α (HIFα) ortholog Sima as a key neuronal transcriptional regulator. Knock-down of sima restores function in several Drosophila models of mitochondrial dysfunction, including models of human disease. Here we discuss these findings and speculate on the potential benefits of inhibition of retrograde signaling. We also describe how our results relate to other studies of mitochondrial retrograde signaling and the potential therapeutic applications of these discoveries.
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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.