ReviewNeurochemical research2023
Mitochondrial Dysfunction and Parkinson's Disease: Pathogenesis and Therapeutic Strategies.
Review in Neurochemical research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers, 1 of them a synthesis 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
72 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.
- Standardized clinical assessments and advanced AI-driven instruments used to evaluate neurofunctional deficits, including within biomarker based framework, in Parkinson's disease - human intelligence made vs. AI models - systematic review.Frontiers in medicine · 2025Pooled it
- Nitric oxide signaling and mitophagy in Parkinson's disease: implications for aerobic exercise-related neuroprotection.Medical gas research · 2027Review
- From neuroinflammation to immune reprogramming: Nanozyme-Integrated nanoplatforms for neuroimmune modulation in Parkinson's disease.Materials today. Bio · 2026Article
- Genetic architecture and molecular pathogenesis of Parkinson's disease: emerging mechanisms and therapeutic targets.Metabolic brain disease · 2026Review
- Mitochondrial Complex V Dysfunction in Neurodegeneration: Secondary Bystander or Primary Driver?Brain sciences · 2026Review
- Article
- BjPro-7a, A Proline-Rich Peptide from Bothrops jararaca Venom, Reverses MPP⁺-Induced Locomotor Deficits and Rescues Mitochondrial, Redox, and Synaptic Proteomic Pathways in a Zebrafish Model of Parkinsonism.Neurochemical research · 2026Article
- Neuroprotective effects of 2-(2-nitrophenyl)-1,3-thiazolidine-4-carboxylic acid in a rotenone-induced Parkinson's disease rat model: Modulation of oxidative stress, behavioral dysfunction, and iron accumulation.Metabolic brain disease · 2026Article
- Review
- Mitochondria-targeted delivery strategies for age-related diseases.International journal of pharmaceutics: X · 2026Review
- Targeting Mitochondria in Aging-Related Diseases: Therapeutic Potential and Obstacles.MedComm · 2026Review
- Stem Cell-Derived Exosomes Regulate Mitochondrial Function: A Novel Strategy for Parkinson's Disease Therapy.Molecular neurobiology · 2026Review
- Neuroprotective Effects ofPharmaceuticals (Basel, Switzerland) · 2026Article
- Mitochondrial Fission and Fusion Disorders and Autophagy Abnormalities in Parkinson's Disease.Neurochemical research · 2026Review
- Redefining Parkinson's Disease management: the synergistic role of neurotrophic factors and mitochondria.Cellular and molecular life sciences : CMLS · 2026Review
- Targeting NME3 to Restore Mitochondrial Fission-Fusion Balance Defines a Novel Disease-Modifying Strategy for Parkinson's Disease.CNS neuroscience & therapeutics · 2026Article
- Potential common pathogenesis of several neurodegenerative diseases.Neural regeneration research · 2026Article
- Targeting oxidative stress and mitochondrial dysfunction via URG7 overexpression in an in vitro Parkinson's disease neuronal model.Scientific reports · 2026Article
- Edible Bird's Nest as a Multi-Component Functional Food for Brain Aging: From Single-Bioactive Actions to Network-Regulatory Mechanisms.Nutrients · 2026Review
- APurinergic signalling · 2026Article
12 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
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Parkinson's disease (PD) is a common age-related neurodegenerative disorder whose pathogenesis is not completely understood. Mitochondrial dysfunction and increased oxidative stress have been considered as major causes and central events responsible for the progressive degeneration of dopaminergic (DA) neurons in PD. Therefore, investigating mitochondrial disorders plays a role in understanding the pathogenesis of PD and can be an important therapeutic target for this disease. This study discusses the effect of environmental, genetic and biological factors on mitochondrial dysfunction and also focuses on the mitochondrial molecular mechanisms underlying neurodegeneration, and its possible therapeutic targets in PD, including reactive oxygen species generation, calcium overload, inflammasome activation, apoptosis, mitophagy, mitochondrial biogenesis, and mitochondrial dynamics. Other potential therapeutic strategies such as mitochondrial transfer/transplantation, targeting microRNAs, using stem cells, photobiomodulation, diet, and exercise were also discussed in this review, which may provide valuable insights into clinical aspects. A better understanding of the roles of mitochondria in the pathophysiology of PD may provide a rationale for designing novel therapeutic interventions in our fight against PD.
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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.