ReviewNPJ Parkinson's disease2022
Mitophagy and reactive oxygen species interplay in Parkinson's disease.
Review in NPJ Parkinson's disease, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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
59 citing papers in PubMed, 98 citations in OpenAlex.
- Oxygen-vacancy-engineered t-ZnO-CeOBioactive materials · 2026Article
- Hypoxia and TTR dysregulation in astrocytes from Parkinson's disease with a specific mitochondrial haplogroup: A single-cell analysis.Neural regeneration research · 2026Article
- FOXO family and neurodegenerative diseases: Mechanisms of action and therapeutic potential.Redox biology · 2026Review
- Mitochondrial Quality Control and Pathogenic Signaling Networks in Parkinson's Disease.Current issues in molecular biology · 2026Review
- An upstream open reading frame regulates expression of the mitochondrial protein Slm35 and mitophagy flux.FEBS letters · 2026Article
- CCL2 and PAK6 as Candidate Biomarkers of Neuroinflammation in Parkinson's Disease: An Integrated Machine Learning and Single-Nucleus Transcriptomic Study.Brain sciences · 2026Article
- Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms.Health science reports · 2026Article
- Energetic diversity in retinal ganglion cells is modulated by neuronal activity and correlates with resilience to degeneration.Nature communications · 2026Article
- HUWE1 regulates mitophagy to protect dopaminergic neurons from 6-OHDA- and MPP⁺-induced neurotoxicity.Cell biology and toxicology · 2026Article
- Superoxide signals for the mitophagy of dysfunctional mitochondria to maintain quality control.Redox biology · 2026Review
- Role of Microglial Dysfunction in Parkinson's Disease: From Multifactorial Causes to Neurodegeneration.Neuroscience bulletin · 2026Review
- Melatonin as a Guardian of Mitochondria: Mechanisms and Therapeutic Potential in Neurodegenerative Diseases.Biology · 2026Review
- Mitophagy-NLRP3 Inflammasome Crosstalk in Parkinson's Disease: Pathogenic Mechanisms and Emerging Therapeutic Strategies.International journal of molecular sciences · 2026Review
- The role of energy deficit in autophagy failure in Parkinson's disease.Frontiers in aging neuroscience · 2026Review
- Engineered extracellular vesicles-mediated curcumin delivery in brain microenvironment modulating lysosomes, mitochondria, and microglia reprogram for parkinson's disease therapy.Journal of nanobiotechnology · 2025Article
- Stress and neurodegeneration: mechanistic insights and therapeutic opportunities for preserving brain resilience.Acta neurologica Belgica · 2025Review
- Nrf2/Keap1 Signaling Axis in the Brain: Master Regulator of Oxidative Stress in Neurodegenerative and Psychiatric Disorders.Molecular neurobiology · 2025Review
- Roles of Autophagy and Oxidative Stress in Cardiovascular Disease.Antioxidants (Basel, Switzerland) · 2025Review
- Targeting macro- and micro-nutrient regulation of HNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- NAD+-Boosters Improve Mitochondria Quality Control In Parkinson's Disease Models Via Mitochondrial UPR.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitophagy impairment and oxidative stress are cardinal pathological hallmarks in Parkinson's disease (PD), a common age-related neurodegenerative condition. The specific interactions between mitophagy and reactive oxygen species (ROS) have attracted considerable attention even though their exact interplay in PD has not been fully elucidated. We highlight the interactions between ROS and mitophagy, with a focus on the signalling pathways downstream to ROS that triggers mitophagy and draw attention to potential therapeutic compounds that target these pathways in both experimental and clinical models. Identifying a combination of ROS inhibitors and mitophagy activators to provide a physiologic balance in this complex signalling pathways may lead to a more optimal outcome. Deciphering the exact temporal relationship between mitophagy and oxidative stress and their triggers early in the course of neurodegeneration can unravel mechanistic clues that potentially lead to the development of compounds for clinical drug trials focusing on prodromic PD or at-risk individuals.
Identifiers
What Socratic 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 Socratic graph.