ArticleAging cell2022
Mitochondrial uncoupling protein-2 reprograms metabolism to induce oxidative stress and myofibroblast senescence in age-associated lung fibrosis.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
What it found
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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
26 citing papers in PubMed, 42 citations in OpenAlex.
- Hallmarks of the ageing lung: 10 years later.The European respiratory journal · 2026Review
- Conditional BCL-2 Expression in Fibroblasts Promotes Persistent Pulmonary Fibrosis which is Reversible by Therapeutic BCL-2 Inhibition.Nature communications · 2026Article
- The Role of Aryl Hydrocarbon Receptor in Airway Remodeling: Mechanistic Insights Across Cellular Functions.Clinical reviews in allergy & immunology · 2026Review
- Deciphering Uncoupling Proteins in Cellular Homeostasis and Metabolic Health.International journal of biological sciences · 2026Review
- Mitochondrial dysfunction in cellular senescence: a bridge to neurodegenerative disease.npj aging · 2025Review
- Taurine in Type 2 Diabetes: Plasma Concentrations, Metabolic Pathways, and Potential as a Therapeutic Adjuvant.Current nutrition reports · 2025Review
- Dysfunctional glycolysis-UCP2-fatty acid oxidation promotes CTLA4Molecular medicine (Cambridge, Mass.) · 2025Article
- Fibroblast activation and heterogeneity in fibrotic disease.Nature reviews. Nephrology · 2025Review
- LPS-Induced Intracellular Complement 3 Activation Regulated ATP Production in Yak Rumen Epithelial Cells.Veterinary sciences · 2025Article
- Regulatory Roles of Long Noncoding RNAs in Arterial Stiffness and Hypertension.Hypertension (Dallas, Tex. : 1979) · 2025Article
- Genipin attenuates oxidative damage in periodontal tissues by alleviating mitochondrial dysfunction and abnormal glucose uptake through inhibition of UCP2.Frontiers in pharmacology · 2025Article
- A novel senolytic drug for pulmonary fibrosis: BTSA1 targets apoptosis of senescent myofibroblasts by activating BAX.Aging cell · 2024Article
- Mechanisms of Bleomycin-induced Lung Fibrosis: A Review of Therapeutic Targets and Approaches.Cell biochemistry and biophysics · 2024Review
- Regulatory Roles of Long Non-Coding RNAs in Arterial Stiffness and Hypertension: Insights from Two African American Studies.bioRxiv : the preprint server for biology · 2024Article
- Inhibition of Distal Glycolytic Enzymes Suppresses Fibroblast Activation without Deleterious Bioenergetic Effects.American journal of respiratory cell and molecular biology · 2024Article
- Cellular Senescence: A Troy Horse in Pulmonary Fibrosis.International journal of molecular sciences · 2023Review
- Histone deacetylase 3 deletion in alveolar type 2 epithelial cells prevents bleomycin-induced pulmonary fibrosis.Clinical epigenetics · 2023Article
- ANT1 and the SASP: Beyond the Bioenergetic Void.American journal of respiratory cell and molecular biology · 2023Article
- Efficient intervention for pulmonary fibrosis via mitochondrial transfer promoted by mitochondrial biogenesis.Nature communications · 2023Article
- Integrating bioinformatic resources to identify characteristics of rheumatoid arthritis-related usual interstitial pneumonia.BMC genomics · 2023Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction has been associated with age-related diseases, including idiopathic pulmonary fibrosis (IPF). We provide evidence that implicates chronic elevation of the mitochondrial anion carrier protein, uncoupling protein-2 (UCP2), in increased generation of reactive oxygen species, altered redox state and cellular bioenergetics, impaired fatty acid oxidation, and induction of myofibroblast senescence. This pro-oxidant senescence reprogramming occurs in concert with conventional actions of UCP2 as an uncoupler of oxidative phosphorylation with dissipation of the mitochondrial membrane potential. UCP2 is highly expressed in human IPF lung myofibroblasts and in aged fibroblasts. In an aging murine model of lung fibrosis, the in vivo silencing of UCP2 induces fibrosis regression. These studies indicate a pro-fibrotic function of UCP2 in chronic lung disease and support its therapeutic targeting in age-related diseases associated with impaired tissue regeneration and organ fibrosis.
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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.