ReviewThe Journal of biological chemistry
Targeting mitophagy in Parkinson's disease.
Review in The Journal of biological chemistry. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers, 2 of them syntheses that pooled it.
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
74 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Systematic review of innate immune responses againstFrontiers in immunology · 2024Pooled it
- Inter-organellar Communication in Parkinson's and Alzheimer's Disease: Looking Beyond Endoplasmic Reticulum-Mitochondria Contact Sites.Frontiers in neuroscience · 2022Pooled it
- Phytogenic Nanoparticles for Parkinson's Disease Therapy: Mechanistic Insights, Brain-Targeted Delivery and Neuroprotective Potential.Molecular neurobiology · 2026Review
- Saffron and its Bioactive Constituents as Mitochondria-Targeted Protectors Against Organ Injury.Molecular neurobiology · 2026Review
- Piezoelectric neuromodulation of the subthalamic nucleus ameliorates motor and nonmotor symptoms of Parkinson's disease.Science advances · 2026Article
- Activation of mitophagy via miR-223/NLRP3 axis ameliorates dopaminergic neuronal damage in parkinson's disease.Metabolic brain disease · 2026Article
- Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review.Current issues in molecular biology · 2026Review
- Disruption of intracellular iron homeostasis through mitochondrial dysfunction associated with suppression of ATP 13A2 expression.Scientific reports · 2026Article
- Systematic discovery of disease-modifying targets by prediction from knowledge graph-based AI model and experimental validation: Parkinson's disease case.Computational and structural biotechnology journal · 2026Article
- An explainable ensemble machine learning model using baseline blood transcriptomics to predict Parkinson's disease motor progression.Frontiers in digital health · 2026Article
- Deciphering the Neuroautophagic Interactome: Molecular Circuits Linking Selective Autophagy to Neuropathological Cascades in Neurological Disorders.International journal of biological sciences · 2026Review
- Mitophagy in the pathogenesis and management of disease.Cell research · 2026Review
- Bridging pleiotropic mechanisms in leprosy type-1 reactions and neurodegenerative diseases.Scientific reports · 2025Article
- Review
- NAD+-Boosters Improve Mitochondria Quality Control In Parkinson's Disease Models Via Mitochondrial UPR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Mitochondrial Aging in the CNS: Unravelling Implications for Neurological Health and Disease.Biomolecules · 2025Review
- Magnetoelectric nanodiscs diminish motor deficits in a model of Parkinson's disease.bioRxiv : the preprint server for biology · 2025Article
- Protein kinases in neurodegenerative diseases: current understandings and implications for drug discovery.Signal transduction and targeted therapy · 2025Review
- Mitochondrial dysfunction, cause or consequence in neurodegenerative diseases?BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- Mitochondrial Dysfunction as a Potential Mechanism Mediating Cardiac Comorbidities in Parkinson's Disease.International journal of molecular sciences · 2024Review
14 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetics and pathophysiology of Parkinson's disease (PD) strongly implicate mitochondria in disease aetiology. Elegant studies over the last two decades have elucidated complex molecular signaling governing the identification and removal of dysfunctional mitochondria from the cell, a process of mitochondrial quality control known as mitophagy. Mitochondrial deficits and specifically reduced mitophagy are evident in both sporadic and familial PD. Mendelian genetics attributes loss-of-function mutations in key mitophagy regulators PINK1 and Parkin to early-onset PD. Pharmacologically enhancing mitophagy and accelerating the removal of damaged mitochondria are of interest for developing a disease-modifying PD therapeutic. However, despite significant understanding of both PINK1-Parkin-dependent and -independent mitochondrial quality control pathways, the therapeutic potential of targeting mitophagy remains to be fully explored. Here, we provide a summary of the genetic evidence supporting the role for mitophagy failure as a pathogenic mechanism in PD. We assess the tractability of mitophagy pathways and prospects for drug discovery and consider intervention points for mitophagy enhancement. We explore the numerous hit molecules beginning to emerge from high-content/high-throughput screening as well as the biochemical and phenotypic assays that enabled these screens. The chemical and biological properties of these reference compounds suggest many could be used to interrogate and perturb mitochondrial biology to validate promising drug targets. Finally, we address key considerations and challenges in achieving preclinical proof-of-concept, including in vivo mitophagy reporter methodologies and disease models, as well as patient stratification and biomarker development for mitochondrial forms of the disease.
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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.