ArticleTranslational neurodegeneration2012
Mitochondrial neuronal uncoupling proteins: a target for potential disease-modification in Parkinson's disease.
Article in Translational neurodegeneration, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 80 citations in OpenAlex.
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- Redox modulatory role of DJ-1 in Parkinson's disease.Biogerontology · 2025Review
- Irisin regulates oxidative stress and mitochondrial dysfunction through the UCP2-AMPK pathway in prion diseases.Cell death & disease · 2025Article
- Parkinson's Disease Dementia Patients: Expression of Glia Maturation Factor in the Brain.International journal of molecular sciences · 2024Article
- Age-associated sex difference in the expression of mitochondria-based redox sensitive proteins and effect of pioglitazone in nonhuman primate brain.Biology of sex differences · 2023Article
- Recent Advances in the Knowledge of the Mechanisms of Leptin Physiology and Actions in Neurological and Metabolic Pathologies.International journal of molecular sciences · 2023Review
- Ginsenoside Rg1 Plays a Neuroprotective Role in Regulating the Iron-Regulated Proteins and Against Lipid Peroxidation in Oligodendrocytes.Neurochemical research · 2022Article
- Food Contamination: An Unexplored Possible Link between Dietary Habits and Parkinson's Disease.Nutrients · 2022Review
- Role of ketone bodies in diabetes-induced dementia: sirtuins, insulin resistance, synaptic plasticity, mitochondrial dysfunction, and neurotransmitter.Nutrition reviews · 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
- Skeletal muscle transcriptomics identifies common pathways in nerve crush injury and ageing.Skeletal muscle · 2022Article
- NRF2 Activation and Downstream Effects: Focus on Parkinson's Disease and Brain Angiotensin.Antioxidants (Basel, Switzerland) · 2021Review
- A Novel Method for Creating a Synthetic L-DOPA Proteome and In Vitro Evidence of Incorporation.Proteomes · 2021Article
- Increasing Nrf2 Activity as a Treatment Approach in Neuropsychiatry.Molecular neurobiology · 2021Review
- PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders.Pharmacology & therapeutics · 2021Review
- Early Onset of Sex-Dependent Mitochondrial Deficits in the Cortex of 3xTg Alzheimer's Mice.Cells · 2020Article
- Role of DJ-1 in the mechanism of pathogenesis of Parkinson's disease.Journal of bioenergetics and biomembranes · 2019Review
- Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.Antioxidants & redox signaling · 2019Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This review gives a brief insight into the role of mitochondrial dysfunction and oxidative stress in the converging pathogenic processes involved in Parkinson's disease (PD). Mitochondria provide cellular energy in the form of ATP via oxidative phosphorylation, but as an integral part of this process, superoxides and other reactive oxygen species are also produced. Excessive free radical production contributes to oxidative stress. Cells have evolved to handle such stress via various endogenous anti-oxidant proteins. One such family of proteins is the mitochondrial uncoupling proteins (UCPs), which are anion carriers located in the mitochondrial inner membrane. There are five known homologues (UCP1 to 5), of which UCP4 and 5 are predominantly expressed in neural cells. In a series of previous publications, we have shown how these neuronal UCPs respond to 1-methyl-4-phenylpyridinium (MPP+; toxic metabolite of MPTP) and dopamine-induced toxicity to alleviate neuronal cell death by preserving ATP levels and mitochondrial membrane potential, and reducing oxidative stress. We also showed how their expression can be influenced by nuclear factor kappa-B (NF-κB) signaling pathway specifically in UCP4. Furthermore, we previously reported an interesting link between PD and metabolic processes through the protective effects of leptin (hormone produced by adipocytes) acting via UCP2 against MPP+-induced toxicity. There is increasing evidence that these endogenous neuronal UCPs can play a vital role to protect neurons against various pathogenic stresses including those associated with PD. Their expression, which can be induced, may well be a potential therapeutic target for various drugs to alleviate the harmful effects of pathogenic processes in PD and hence modify the progression of this disease.
Identifiers
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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.