ArticleNature communications2015
Increased COUP-TFII expression in adult hearts induces mitochondrial dysfunction resulting in heart failure.
Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 72 citations in OpenAlex.
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- Hells protects mitochondrial integrity via Nr2f2 suppression during osteoclast differentiation.Cell communication and signaling : CCS · 2026Article
- Emerging Mechanisms and Therapeutic Strategies in Dilated Cardiomyopathy.Biomedicines · 2026Review
- Repurposing of lansoprazole and nitazoxanide as NR2F2 inhibitors in the gastric cancer cell line GCIY: computational insights and siRNA-mediatedFrontiers in chemistry · 2026Article
- Inhibition of NR2F2 suppresses invasion ability and modulates EMT marker in head and neck squamous cell carcinoma.Discover oncology · 2025Article
- Role of COUP‑TFII in cardiovascular diseases and colorectal cancer: Insights into the molecular mechanisms and clinical relevance (Review).Molecular medicine reports · 2025Review
- Single-vessel transcriptome map pathological landscapes and reveal NR2F2-mediated smooth muscle cell phenotype acquisition in capillary malformations.bioRxiv : the preprint server for biology · 2025Article
- Activating nuclear receptor subfamily 2 group F member 2 in adipocyte stem cells rescues beige adipocyte metabolism impaired by excess early-life omega-6 fatty acids.Clinical nutrition (Edinburgh, Scotland) · 2025Article
- Targeting the DNA damage response (DDR) of cancer cells with natural compounds derived fromJournal of ginseng research · 2025Review
- Omics Studies of Specialized Cells and Stem Cells under Microgravity Conditions.International journal of molecular sciences · 2024Review
- NR2F2 alleviates pulmonary fibrosis by inhibition of epithelial cell senescence.Respiratory research · 2024Article
- The lncRNA lnc_AABR07044470.1 promotes the mitochondrial-damaged inflammatory response to neuronal injury via miR-214-3p/PERM1 axis in acute ischemic stroke.Molecular biology reports · 2024Article
- Astragaloside IV attenuates sunitinib-associated cardiotoxicity by inhibiting COUP-TFII.Heliyon · 2024Article
- Reduced NR2F2 Expression in the Host Response to Infectious Bursal Disease Virus Infection Suppressed Viral Replication by Enhancing Type I Interferon Expression by Targeting SOCS5.Journal of virology · 2023Article
- Brain nuclear receptors and cardiovascular function.Cell & bioscience · 2023Review
- Mitochondrial Dysfunction and Therapeutic Perspectives in Cardiovascular Diseases.International journal of molecular sciences · 2022Review
- An NKX-COUP-TFII morphogenetic code directs mucosal endothelial addressin expression.Nature communications · 2022Article
- Transcriptional control of energy metabolism by nuclear receptors.Nature reviews. Molecular cell biology · 2022Review
- Single-cell genomic profiling of human dopamine neurons identifies a population that selectively degenerates in Parkinson's disease.Nature neuroscience · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 1 country.
Funding
Abstract
Mitochondrial dysfunction and metabolic remodelling are pivotal in the development of cardiomyopathy. Here, we show that myocardial COUP-TFII overexpression causes heart failure in mice, suggesting a causal effect of elevated COUP-TFII levels on development of dilated cardiomyopathy. COUP-TFII represses genes critical for mitochondrial electron transport chain enzyme activity, oxidative stress detoxification and mitochondrial dynamics, resulting in increased levels of reactive oxygen species and lower rates of oxygen consumption in mitochondria. COUP-TFII also suppresses the metabolic regulator PGC-1 network and decreases the expression of key glucose and lipid utilization genes, leading to a reduction in both glucose and oleate oxidation in the hearts. These data suggest that COUP-TFII affects mitochondrial function, impairs metabolic remodelling and has a key role in dilated cardiomyopathy. Last, COUP-TFII haploinsufficiency attenuates the progression of cardiac dilation and improves survival in a calcineurin transgenic mouse model, indicating that COUP-TFII may serve as a therapeutic target for the treatment of dilated cardiomyopathy.
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Registered trials
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