ArticleBrain and behavior2012
Human neuronal uncoupling proteins 4 and 5 (UCP4 and UCP5): structural properties, regulation, and physiological role in protection against oxidative stress and mitochondrial dysfunction.
Article in Brain and behavior, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
63 citing papers in PubMed, 1 synthesis or guideline pooled it, 124 citations in OpenAlex.
- Ethnicity Differences in the Association of UCP1-3826A/G, UCP2-866G/A and Ala55Val, and UCP3-55C/T Polymorphisms with Type 2 Diabetes Mellitus Susceptibility: An Updated Meta-Analysis.BioMed research international · 2021Pooled it
- Mitochondrial Dynamics and SLC25 Transporters in Neurodegeneration: From Mechanisms to Therapeutic Opportunities.Biomolecules · 2026Review
- Targeting mitochondrial transporters and metabolic reprogramming for disease treatment.Journal of translational medicine · 2025Review
- Effects of nutrients and diet on mitochondrial dysfunction: An opportunity for therapeutic approaches in human disease.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2025Review
- Epicatechin DecreasesInternational journal of molecular sciences · 2025Article
- Attention-deficit hyperactivity disorder in spontaneously hypertensive rat strain SHR/NCrl is associated with specific expression of uncoupling proteins, glucose transporter 1 and BACE1.Frontiers in cellular neuroscience · 2025Article
- A New Strategy for Targeting UCP2 to Modulate Glycolytic Reprogramming as a Treatment for Sepsis A New Strategy for Targeting UCP2.Inflammation · 2024Review
- Prenatal immune activation in mice induces long-term alterations in brain mitochondrial function.Translational psychiatry · 2024Article
- Mitochondrial uncoupling proteins protect human airway epithelial ciliated cells from oxidative damage.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Review
- Ucp4 Knockdown of Cerebellar Purkinje Cells Induces Bradykinesia.Molecular neurobiology · 2024Article
- Review
- Unveiling the Role of the Proton Gateway, Uncoupling Proteins (UCPs), in Cancer Cachexia.Cancers · 2023Review
- Lipid Adaptations against Oxidative Challenge in the Healthy Adult Human Brain.Antioxidants (Basel, Switzerland) · 2023Review
- The Cholinergic Pathway and MitoKStroke (Hoboken, N.J.) · 2022Article
- Pyruvate Dehydrogenase Kinase Protects Dopaminergic Neurons from Oxidative Stress inMolecules and cells · 2022Article
- Protective Role of Mitochondrial Uncoupling Proteins against Age-Related Oxidative Stress in Type 2 Diabetes Mellitus.Antioxidants (Basel, Switzerland) · 2022Review
- Uncoupling Proteins as Therapeutic Targets for Neurodegenerative Diseases.International journal of molecular sciences · 2022Review
- Skeletal Muscle Uncoupling Proteins in Mice Models of Obesity.Metabolites · 2022Review
- Role of ketone bodies in diabetes-induced dementia: sirtuins, insulin resistance, synaptic plasticity, mitochondrial dysfunction, and neurotransmitter.Nutrition reviews · 2022Review
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
8 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Uncoupling proteins (UCPs) belong to a large family of mitochondrial solute carriers 25 (SLC25s) localized at the inner mitochondrial membrane. UCPs transport protons directly from the intermembrane space to the matrix. Of five structural homologues (UCP1 to 5), UCP4 and 5 are principally expressed in the central nervous system (CNS). Neurons derived their energy in the form of ATP that is generated through oxidative phosphorylation carried out by five multiprotein complexes (Complexes I-V) embedded in the inner mitochondrial membrane. In oxidative phosphorylation, the flow of electrons generated by the oxidation of substrates through the electron transport chain to molecular oxygen at Complex IV leads to the transport of protons from the matrix to the intermembrane space by Complex I, III, and IV. This movement of protons to the intermembrane space generates a proton gradient (mitochondrial membrane potential; MMP) across the inner membrane. Complex V (ATP synthase) uses this MMP to drive the conversion of ADP to ATP. Some electrons escape to oxygen-forming harmful reactive oxygen species (ROS). Proton leakage back to the matrix which bypasses Complex V resulting in a major reduction in ROS formation while having a minimal effect on MMP and hence, ATP synthesis; a process termed "mild uncoupling." UCPs act to promote this proton leakage as means to prevent excessive build up of MMP and ROS formation. In this review, we discuss the structure and function of mitochondrial UCPs 4 and 5 and factors influencing their expression. Hypotheses concerning the evolution of the two proteins are examined. The protective mechanisms of the two proteins against neurotoxins and their possible role in regulating intracellular calcium movement, particularly with regard to the pathogenesis of Parkinson's disease are discussed.
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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.