ArticleMolecules and cells2016
Uncoupling Protein, UCP-4 May Be Involved in Neuronal Defects During Aging and Resistance to Pathogens in Caenorhabditis elegans.
Article in Molecules and cells, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 16 citations in OpenAlex.
- Specialized high-capacity mitochondria fuel cell invasion.Current biology : CB · 2026Article
- The mitochondrial uncoupling proteins in early-branching animals: comparative analysis and transcriptional response to temperature in the jellyfish Stomolophus sp.2.Journal of bioenergetics and biomembranes · 2025Article
- ElixirSeeker: A Machine Learning Framework Utilizing Fusion Molecular Fingerprints for the Discovery of Lifespan-Extending Compounds.Aging cell · 2025Article
- Exploring the role of mitochondrial uncoupling protein 4 in brain metabolism: implications for Alzheimer's disease.Frontiers in neuroscience · 2024Review
- Preservation of mitochondrial membrane potential is necessary for lifespan extension from dietary restriction.GeroScience · 2023Article
- Comprehensive Analysis and Validation of Solute Carrier Family 25 (SLC25) and Its Correlation with Immune Infiltration in Pan-Cancer.BioMed research international · 2022Article
- Flavonoids mitigate neurodegeneration in agedFood science & nutrition · 2020Article
- Tart Cherry Increases Lifespan inNutrients · 2020Article
- 20,000 picometers under the OMM: diving into the vastness of mitochondrial metabolite transport.EMBO reports · 2020Review
- Mitochondrial Uncoupling Attenuates Age-Dependent Neurodegeneration in C. elegans.Molecules and cells · 2017Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uncoupling proteins (UCPs) are mitochondrial inner membrane proteins that function to dissipate proton motive force and mitochondrial membrane potential. One UCP has been identified in Caenorhabditis elegans (C. elegans), namely UCP-4. In this study, we examined its expression and localization using a GFP marker in C. elegans. ucp-4 was expressed throughout the body from early embryo to aged adult and UCP-4 was localized in the mitochondria. It is known that increased mitochondrial membrane protential leads to a reactive oxygen species (ROS) increase, which is associated with age-related diseases, including neurodegenerative diseases in humans. A ucp-4 mutant showed increased mitochondrial membrane protential in association with increased neuronal defects during aging, and the neurons of ucp-4 overexpressing animals showed decreased neuronal defects during aging. These results suggest that UCP-4 may be involved in neuroprotection during aging via relieving mitochondrial membrane protential. We also investigated the relationship between UCP-4 and innate immunity because increased ROS can affect innate immunity. ucp-4 mutant displayed increased resistance to the pathogen Staphylococcus aureus compared to wild type. The enhanced immunity in the ucp-4 mutant could be related to increased mitochondrial membrane protential, presumably followed by increased ROS. In summary, UCP-4 might have an important role in neuronal aging and innate immune responses through mediating mitochondrial membrane protential.
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