ArticlePLoS genetics2014
Loss of UCP2 attenuates mitochondrial dysfunction without altering ROS production and uncoupling activity.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- OSW-1 inhibits tumor cell proliferation and migration via uncoupling protein 2 in hepatocellular carcinoma.Oncology letters · 2025Article
- Mechanism Analysis of UCP2 During the Oxidative Stress Injury of Intestinal Porcine Epithelial Cell Line-J2.Animals : an open access journal from MDPI · 2025Article
- Effect of early vs. late time-restricted high-fat feeding on circadian metabolism and weight loss in obese mice.Cellular and molecular life sciences : CMLS · 2023Article
- Role of UCP2 in the Energy Metabolism of the Cancer Cell Line A549.International journal of molecular sciences · 2023Article
- UCP2 as a Cancer Target through Energy Metabolism and Oxidative Stress Control.International journal of molecular sciences · 2022Review
- Progeria and Aging-Omics Based Comparative Analysis.Biomedicines · 2022Article
- Premature aging is associated with higher levels of 8-oxoguanine and increased DNA damage in the Polg mutator mouse.Aging cell · 2022Article
- Mitochondrial uncoupling protein-2 reprograms metabolism to induce oxidative stress and myofibroblast senescence in age-associated lung fibrosis.Aging cell · 2022Article
- FGF21 modulates mitochondrial stress response in cardiomyocytes only under mild mitochondrial dysfunction.Science advances · 2022Article
- Fetal Cardiac Lipid Sensing Triggers an Early and Sex-related Metabolic Energy Switch in Intrauterine Growth Restriction.The Journal of clinical endocrinology and metabolism · 2021Article
- Phytomodulatory proteins isolated from Calotropis procera latex promote glycemic control by improving hepatic mitochondrial function in HepG2 cells.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2021Article
- Antioxidant Synergy of Mitochondrial Phospholipase PNPLA8/iPLA2γ with Fatty Acid-Conducting SLC25 Gene Family Transporters.Antioxidants (Basel, Switzerland) · 2021Review
- PPARγ/PGC1α signaling as a potential therapeutic target for mitochondrial biogenesis in neurodegenerative disorders.Pharmacology & therapeutics · 2021Review
- UCP2 as a Potential Biomarker for Adjunctive Metabolic Therapies in Tumor Management.Frontiers in oncology · 2021Review
- Mitochondrial Dysfunction: a Potential Therapeutic Target to Treat Alzheimer's Disease.Molecular neurobiology · 2020Review
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
- Alterations in Glucose Metabolism During the Transition to Heart Failure: The Contribution of UCP-2.Cells · 2020Article
- Mice deficient in pyruvate dehydrogenase kinase 4 are protected against acetaminophen-induced hepatotoxicity.Toxicology and applied pharmacology · 2020Article
- UCP2-induced hypoxia promotes lipid accumulation and tubulointerstitial fibrosis during ischemic kidney injury.Cell death & disease · 2020Article
- FGF21: An Emerging Therapeutic Target for Non-Alcoholic Steatohepatitis and Related Metabolic Diseases.Frontiers in endocrinology · 2020Review
Corrections and comments
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Authors and funding
17 authors at 8 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although mitochondrial dysfunction is often accompanied by excessive reactive oxygen species (ROS) production, we previously showed that an increase in random somatic mtDNA mutations does not result in increased oxidative stress. Normal levels of ROS and oxidative stress could also be a result of an active compensatory mechanism such as a mild increase in proton leak. Uncoupling protein 2 (UCP2) was proposed to play such a role in many physiological situations. However, we show that upregulation of UCP2 in mtDNA mutator mice is not associated with altered proton leak kinetics or ROS production, challenging the current view on the role of UCP2 in energy metabolism. Instead, our results argue that high UCP2 levels allow better utilization of fatty acid oxidation resulting in a beneficial effect on mitochondrial function in heart, postponing systemic lactic acidosis and resulting in longer lifespan in these mice. This study proposes a novel mechanism for an adaptive response to mitochondrial cardiomyopathy that links changes in metabolism to amelioration of respiratory chain deficiency and longer lifespan.
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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.