ArticleAutophagy2016
An unconventional pathway for mitochondrial protein degradation.
Article in Autophagy, 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
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
7 citing papers in PubMed.
- A p-Tyr42 RhoA Inhibitor Promotes the Regeneration of Human Corneal Endothelial Cells by Ameliorating Cellular Senescence.Antioxidants (Basel, Switzerland) · 2023Article
- Mitophagy Improves Ethanol Tolerance in Yeast: Regulation by Mitochondrial Reactive Oxygen Species inJournal of microbiology and biotechnology · 2020Article
- Observational
- Proteome turnover in the bloodstream and procyclic forms ofWellcome open research · 2019Article
- Review
- Role of autophagy in the pathogenesis of inflammatory bowel disease.World journal of gastroenterology · 2017Review
- Involvement of PINK1/parkin-mediated mitophagy in ZnO nanoparticle-induced toxicity in BV-2 cells.International journal of nanomedicine · 2017Article
Corrections and comments
- Comment on
Authors and funding
2 authors.
Funding
Abstract
Many vital metabolic pathways take place in mitochondria, but some of the associated processes generate toxic substances including reactive oxygen species that can damage proteins and DNA. Therefore, it is critical to maintain normally functioning mitochondria to achieve proper cellular homeostasis. Along these lines, mitochondrial dysfunction is associated with numerous diseases, and mitochondria quality control is essential for cell survival. The maintenance of functioning mitochondria is particularly important in aging cells, and there is a strong relationship between cellular aging and dysfunctional mitochondria. The best characterized pathway that is responsible for the elimination of damaged mitochondria is mitophagy, a selective type of autophagy. In yeast, mitophagy requires the mitochondrial protein Atg32 to serve as a receptor for recognition and sequestration by a phagophore. Although conventional mitophagy has been extensively studied, recent research suggests that an unconventional pathway, which is independent of Atg32, contributes to the removal of mitochondria.
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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.