ArticleInternational journal of molecular sciences2020
miR-218 Inhibits Mitochondrial Clearance by Targeting PRKN E3 Ubiquitin Ligase.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.
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Who cites it
31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 40 citations in OpenAlex.
- The Intersection of Mitophagy and Autism Spectrum Disorder: A Systematic Review.International journal of molecular sciences · 2025Pooled it
- Deregulated mitochondrial microRNAs in Alzheimer's disease: Focus on synapse and mitochondria.Ageing research reviews · 2022Pooled it
- The Diagnostic and Therapeutic Value of Micro-RNA in Parkinson's Disease.Cellular and molecular neurobiology · 2026Review
- Mitochondria-Associated MicroRNAs: Emerging Roles in the Pathogenesis of Parkinson's Disease.Biomedicines · 2026Review
- Host miRNA orchestration of mitophagy pathways during bacterial infection: current advances and future directions.Frontiers in microbiology · 2026Review
- PRKN Ser131 phosphorylation promotes cigarette smoke-induced mitophagy impairment and epithelial cell senescence via MKK3/p38 MAPK activation: An in vitro and in vivo study.Tobacco induced diseases · 2026Article
- Mitochondrial dysfunction as a key player in aggravating periodontitis among diabetic patients: review of the current scope of knowledge.Naunyn-Schmiedeberg's archives of pharmacology · 2025Review
- Advances in miRNA research: Unraveling the complexities of gene regulation.Animal models and experimental medicine · 2025Review
- Bioenergetic failure and oxidative stress: mitochondrial contributions to Alzheimer's disease.Inflammopharmacology · 2025Review
- Unlocking Parkinson's disease: the role of microRNAs in regulation, diagnosis, and therapy.Apoptosis : an international journal on programmed cell death · 2025Review
- Exploring the Mechanisms and Therapeutic Approaches of Mitochondrial Dysfunction in Alzheimer's Disease: An Educational Literature Review.Molecular neurobiology · 2025Review
- A Narrative Review Evaluating Diet and Exercise as Complementary Medicine for the Management of Alzheimer's Disease.Nutrients · 2025Review
- Mitochondrial microRNAs: Key Drivers in Unraveling Neurodegenerative Diseases.International journal of molecular sciences · 2025Review
- Mitochondrial microRNAs (mitomiRs) as emerging biomarkers and therapeutic targets for chronic human diseases.Frontiers in genetics · 2025Review
- The Mitochondrial Blueprint: Unlocking Secondary Metabolite Production.Metabolites · 2024Review
- MicroRNAs regulation in Parkinson's disease, and their potential role as diagnostic and therapeutic targets.NPJ Parkinson's disease · 2024Review
- Stress-Related Roles of Exosomes and Exosomal miRNAs in Common Neuropsychiatric Disorders.International journal of molecular sciences · 2024Review
- miR-218-5p and doxorubicin combination enhances anticancer activity in breast cancer cells through Parkin-dependent mitophagy inhibition.Cell death discovery · 2024Article
- Parkin-Mediated Mitophagy by TGF-β Is Connected with Hepatic Stellate Cell Activation.International journal of molecular sciences · 2023Article
- Study on the Role of Mitophagy Receptor PHB2 in Doubly Uniparental Inheritance of Hyriopsis cumingii.Marine biotechnology (New York, N.Y.) · 2023Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The selective elimination of dysfunctional mitochondria through mitophagy is crucial for preserving mitochondrial quality and cellular homeostasis. The most described mitophagy pathway is regulated by a positive ubiquitylation feedback loop in which the PINK1 (PTEN induced kinase 1) kinase phosphorylates both ubiquitin and the E3 ubiquitin ligase PRKN (Parkin RBR E3 ubiquitin ligase), also known as PARKIN. This event recruits PRKN to the mitochondria, thus amplifying ubiquitylation signal. Here we report that miR-218 targets PRKN and negatively regulates PINK1/PRKN-mediated mitophagy. Overexpression of miR-218 reduces PRKN mRNA levels, thus also reducing protein content and deregulating the E3 ubiquitin ligase action. In fact, following miR-218 overexpression, mitochondria result less ubiquitylated and the autophagy machinery fails to proceed with correct mitochondrial clearance. Since mitophagy defects are associated with various human diseases, these results qualify miR-218 as a promising therapeutic target for human diseases.
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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.