ArticleCell proliferation2021
PINK1-mediated mitophagy maintains pluripotency through optineurin.
Article in Cell proliferation, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- NOP2-mediated m5C methylation impairs mitophagy and aggravates acute lung injury by targeting PINK1.Scientific reports · 2026Article
- Mitochondria and pluripotency: from established models to emerging roles in adult stem cells.Frontiers in bioengineering and biotechnology · 2025Review
- Preserving mitochondrial homeostasis protects against drug-induced liver injury via inducing OPTN (optineurin)-dependent Mitophagy.Autophagy · 2024Article
- Autophagy accompanying the developmental process of male germline stem cells.Cell and tissue research · 2024Review
- Review
- Role of CELF2 in ferroptosis: Potential targets for cancer therapy (Review).International journal of molecular medicine · 2023Review
- Bendless is essential for PINK1-Park mediated Mitofusin degradation under mitochondrial stress caused by loss of LRPPRC.PLoS genetics · 2023Article
- Mitochondrial regulation in human pluripotent stem cells during reprogramming and β cell differentiation.Frontiers in endocrinology · 2023Review
- BNIP3-dependent mitophagy safeguards ESC genomic integrity via preventing oxidative stress-induced DNA damage and protecting homologous recombination.Cell death & disease · 2022Article
- Evaluating mitophagy in embryonic stem cells by using fluorescence-based imaging.Frontiers in cell and developmental biology · 2022Article
- Therapeutic application of quercetin in aging-related diseases: SIRT1 as a potential mechanism.Frontiers in immunology · 2022Review
- Nutrients in the fate of pluripotent stem cells.Cell metabolism · 2021Review
- PINK1-mediated mitophagy maintains pluripotency through optineurin.Cell proliferation · 2021Article
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 1 country.
Funding
Abstract
objectivesDysfunction of autophagy results in accumulation of depolarized mitochondria and breakdown of self-renewal and pluripotency in ESCs. However, the regulators that control how mitochondria are degraded by autophagy for pluripotency regulation remains largely unknown. This study aims to dissect the molecular mechanisms that regulate mitochondrial homeostasis for pluripotency regulation in mouse ESCs. MATERIALS AND
methodsParkin
resultsPINK1 or OPTN depletion impairs the degradation of dysfunctional mitochondria during reprogramming, and reduces the reprogramming efficiency and quality. In ESCs, PINK1 or OPTN deficiency leads to accumulation of dysfunctional mitochondria and compromised pluripotency. The defective mitochondrial homeostasis and pluripotency in pink1
conclusionsThe mitophagy receptor OPTN guards ESC mitochondrial homeostasis and pluripotency by scavenging damaged mitochondria through TBK1-activated OPTN binding of PINK1-phosphorylated Ubiquitin.
Indexed as
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.