ReviewInternational journal of molecular sciences2015
Mitochondria: A Therapeutic Target for Parkinson's Disease?
Review in International journal of molecular sciences, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 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
63 citing papers in PubMed, 104 citations in OpenAlex.
- 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
- Evaluation of the neurotrophic peptide mixture in pathogenetic therapy of patients with Parkinson's disease.NPJ Parkinson's disease · 2026Article
- Neuroinflammatory Mechanisms and Vocalization Biomarkers in theMedical research archives · 2025Article
- Adenine Nucleotide Translocase 1 Promotes Functional Integrity of Mitochondria via Activating DDIT3-CytC Pathway and Intensifying Actin Filament Structures.Molecular neurobiology · 2025Article
- Modulation of OPC Mitochondrial Function by Inhibiting USP30 Promotes Their Differentiation.Glia · 2025Article
- Novel and experimental therapeutics for the management of motor and non-motor Parkinsonian symptoms.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2024Review
- Parkinson's Disease: Cells Succumbing to Lifelong Dopamine-Related Oxidative Stress and Other Bioenergetic Challenges.International journal of molecular sciences · 2024Review
- STAT3 protects dopaminergic neurons against degeneration in animal model of Parkinson's disease.Brain research · 2024Article
- Nicotinamide ameliorates mitochondria-related neuronal apoptosis and cognitive impairment via the NADSchizophrenia (Heidelberg, Germany) · 2023Article
- Limonene, a Monoterpene, Mitigates Rotenone-Induced Dopaminergic Neurodegeneration by Modulating Neuroinflammation, Hippo Signaling and Apoptosis in Rats.International journal of molecular sciences · 2023Article
- The Therapeutic Potential of Mitochondria Transplantation Therapy in Neurodegenerative and Neurovascular Disorders.Current neuropharmacology · 2023Review
- Review
- SIRT3 expression alleviates microglia activation‑induced dopaminergic neuron injury through the mitochondrial pathway.Experimental and therapeutic medicine · 2022Article
- Pink1/Parkin-Mediated Mitophagy Regulated the Apoptosis of Dendritic Cells in Sepsis.Inflammation · 2022Article
- Atypical Ubiquitination and Parkinson's Disease.International journal of molecular sciences · 2022Review
- Comparison of the effect of rotenone and 1‑methyl‑4‑phenyl‑1,2,3,6‑tetrahydropyridine on inducing chronic Parkinson's disease in mouse models.Molecular medicine reports · 2022Article
- Dietary Plant Polyphenols as the Potential Drugs in Neurodegenerative Diseases: Current Evidence, Advances, and Opportunities.Oxidative medicine and cellular longevity · 2022Review
- Brain-enriched miR-128: Reduced in exosomes from Parkinson's patient plasma, improves synaptic integrity, and prevents 6-OHDA mediated neuronal apoptosis.Frontiers in cellular neuroscience · 2022Article
- Role of mitophagy in the neurodegenerative diseases and its pharmacological advances: A review.Frontiers in molecular neuroscience · 2022Review
- Mitochondrial Dysregulation and the Influence in Neurodegenerative Diseases.Advances in experimental medicine and biology · 2022Article
3 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 at 2 institutions in 1 country.
Funding
Abstract
Parkinson's disease (PD) is one of the most common neurodegenerative disorders. The exact causes of neuronal damage are unknown, but mounting evidence indicates that mitochondrial-mediated pathways contribute to the underlying mechanisms of dopaminergic neuronal cell death both in PD patients and in PD animal models. Mitochondria are organized in a highly dynamic tubular network that is continuously reshaped by opposing processes of fusion and fission. Defects in either fusion or fission, leading to mitochondrial fragmentation, limit mitochondrial motility, decrease energy production and increase oxidative stress, thereby promoting cell dysfunction and death. Thus, the regulation of mitochondrial dynamics processes, such as fusion, fission and mitophagy, represents important mechanisms controlling neuronal cell fate. In this review, we summarize some of the recent evidence supporting that impairment of mitochondrial dynamics, mitophagy and mitochondrial import occurs in cellular and animal PD models and disruption of these processes is a contributing mechanism to cell death in dopaminergic neurons. We also summarize mitochondria-targeting therapeutics in models of PD, proposing that modulation of mitochondrial impairment might be beneficial for drug development toward treatment of PD.
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.