ArticleScientific reports2021
Mitochondria-affecting small molecules ameliorate proteostasis defects associated with neurodegenerative diseases.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Box C/D snoRNPs and MDT-15/MED15 regulate mitochondrial surveillance and mitophagy via fatty acid metabolism.GeroScience · 2026Article
- Article
- Cerebral Ischemia-Reperfusion Injury: Unraveling the Mitophagy-Oxidative Stress Axis for Neuroprotective Strategies.International journal of molecular sciences · 2026Review
- Putative PINK1/Parkin activators lower the threshold for mitophagy by sensitizing cells to mitochondrial stress.Science advances · 2025Article
- Review
- Mitochondrial Quality Control in Alzheimer's Disease: Insights fromAntioxidants (Basel, Switzerland) · 2024Review
- Mitochondrial abnormalities as a target of intervention in acute myeloid leukemia.Frontiers in oncology · 2024Review
- Targeting mitophagy for neurological disorders treatment: advances in drugs and non-drug approaches.Naunyn-Schmiedeberg's archives of pharmacology · 2023Review
- Noncoupled Mitochondrial Respiration as Therapeutic Approach for the Treatment of Metabolic Diseases: Focus on Transgenic Animal Models.International journal of molecular sciences · 2023Review
- Examining Sporadic Cancer Mutations Uncovers a Set of Genes Involved in Mitochondrial Maintenance.Genes · 2023Article
- The emergent role of mitochondrial surveillance in cellular health.Aging cell · 2022Review
- Mitochondrial Quality Control Mechanisms during Diabetic Cardiomyopathy.JMA journal · 2022Review
- Article
- Prescription drugs and mitochondrial metabolism.Bioscience reports · 2022Review
- Meta-Analysis ofFrontiers in microbiology · 2022Article
- Defective PTEN-induced kinase 1/Parkin mediated mitophagy and neurodegenerative diseases.Frontiers in cellular neuroscience · 2022Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Macroautophagic recycling of dysfunctional mitochondria, known as mitophagy, is essential for mitochondrial homeostasis and cell viability. Accumulation of defective mitochondria and impaired mitophagy have been widely implicated in many neurodegenerative diseases, and loss-of-function mutations of PINK1 and Parkin, two key regulators of mitophagy, are amongst the most common causes of heritable parkinsonism. This has led to the hypothesis that pharmacological stimulation of mitophagy may be a feasible approach to combat neurodegeneration. Toward this end, we screened ~ 45,000 small molecules using a high-throughput, whole-organism, phenotypic screen that monitored accumulation of PINK-1 protein, a key event in mitophagic activation, in a Caenorhabditis elegans strain carrying a Ppink-1::PINK-1::GFP reporter. We obtained eight hits that increased mitochondrial fragmentation and autophagosome formation. Several of the compounds also reduced ATP production, oxygen consumption, mitochondrial mass, and/or mitochondrial membrane potential. Importantly, we found that treatment with two compounds, which we named PS83 and PS106 (more commonly known as sertraline) reduced neurodegenerative disease phenotypes, including delaying paralysis in a C. elegans β-amyloid aggregation model in a PINK-1-dependent manner. This report presents a promising step toward the identification of compounds that will stimulate mitochondrial turnover.
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Registered trials
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