ReviewNeuron2015
The roles of PINK1, parkin, and mitochondrial fidelity in Parkinson's disease.
Review in Neuron, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1,401 papers, 2 of them syntheses that pooled it.
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
1,401 citing papers in PubMed, 2 syntheses or guidelines pooled it, 2,161 citations in OpenAlex.
- N-acetylcysteine for Parkinson's disease: a translational systematic review of mechanistic and early clinical data.Neurodegenerative disease management · 2026Pooled it
- Pooled it
- PINK1 deficiency exacerbates age-related bone loss in association with enhanced inflammatory adipocyte differentiation.Genes & diseases · 2027Article
- Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection.Medical gas research · 2027Review
- The gut microbiome and mitochondrial function in metabolism, immunity, and disease.Gut microbes · 2026Review
- Drosophila dendrites are resilient to adult-onset deficits in mitochondrial dynamics.The Journal of cell biology · 2026Article
- Lactoferrin-modified MSC-derived extracellular vesicles facilitate BBB penetration and enhance gastrodin-induced neuroprotection in Parkinson's disease: involvement of mitophagy.International journal of pharmaceutics: X · 2026Article
- An FGF21-based fusion protein ameliorates mitochondrial dysfunction and promotes recovery post spinal cord injury.Materials today. Bio · 2026Article
- 3C suppresses PINK1-mediated mitophagy and contributes to coxsackievirus B3 replication.Virulence · 2026Article
- The ubiquitin system in heart and vessel pathobiology: From mechanisms to therapeutic strategies.Genes & diseases · 2026Review
- CHCHD2 mitigates age-associated proteostatic collapse by maintaining homeostasis of the mitochondria-lysosome axis.Acta neuropathologica · 2026Article
- Mitochondrial quality control in health and disease: Updates 2026.Chinese medical journal · 2026Review
- Arsenic Exposure Induces Hepatic Fibrosis and Triggers Early Inflammatory Responses by Inhibiting Hepatic Stellate Cell PINK1/Parkin-Mediated Mitophagy.Biological trace element research · 2026Article
- Peripheral Immune Alterations and T Cell Clonal Dynamics Across the Parkinson's Disease Spectrum.medRxiv : the preprint server for health sciences · 2026Article
- Review
- Species-dependent activities of the PINK1-parkin axis.Translational neurodegeneration · 2026Review
- Cholesterol maintains the degradative capacity of lysosomes during clearance and recycling of dysfunctional mitochondria.Nature communications · 2026Article
- Review
- Mitochondrial Quality Control Imbalance in the Heterogeneity of Parkinson's Disease: From Selective Vulnerability to Stratified Transformation.International journal of molecular sciences · 2026Review
- Review
1,341 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
2 authors at 1 institution in 1 country.
Funding
Abstract
Understanding the function of genes mutated in hereditary forms of Parkinson's disease yields insight into disease etiology and reveals new pathways in cell biology. Although mutations or variants in many genes increase the susceptibility to Parkinson's disease, only a handful of monogenic causes of parkinsonism have been identified. Biochemical and genetic studies reveal that the products of two genes that are mutated in autosomal recessive parkinsonism, PINK1 and Parkin, normally work together in the same pathway to govern mitochondrial quality control, bolstering previous evidence that mitochondrial damage is involved in Parkinson's disease. PINK1 accumulates on the outer membrane of damaged mitochondria, activates Parkin's E3 ubiquitin ligase activity, and recruits Parkin to the dysfunctional mitochondrion. Then, Parkin ubiquitinates outer mitochondrial membrane proteins to trigger selective autophagy. This review covers the normal functions that PINK1 and Parkin play within cells, their molecular mechanisms of action, and the pathophysiological consequences of their loss.
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.