ArticleThe Journal of clinical investigation2023
RIP140 deficiency enhances cardiac fuel metabolism and protects mice from heart failure.
Article in The Journal of clinical investigation, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Diet-Associated Regulation of Cardiac Metabolism: Molecular Determinants and Pathophysiological Consequences.Nutrients · 2026Review
- mTORC1 and nuclear ERK spatially control translation in cardiomyocytes through 4EBP1 phosphorylation.Science signaling · 2026Article
- Short-term time-restricted feeding improves metabolic rhythms and liver mitochondrial bioenergetic function in high-fat diet-fed mice.Function (Oxford, England) · 2026Article
- Endothelial ZBTB16: a molecular shield against cardiac aging.European heart journal · 2026Article
- Transcriptome remodeling of mouse hearts during postnatal cardiac maturation and under proteotoxic stress.Molecular biology reports · 2026Article
- An NRIP1-Centric Monocyte Immunogenetic Bridge Between Heart Failure and Ischemic Stroke.Journal of inflammation research · 2026Article
- Crosstalk between microRNAs and autophagy in adipocyte differentiation: emerging therapeutic targets for obesity.Adipocyte · 2025Review
- A role for the transcriptional coregulator RIP140 in the control of muscle endurance fitness.JCI insight · 2025Article
- Whole body MondoA deletion protects against diet-induced obesity through uncontrolled multi-organ substrate utilization and futile cycling.bioRxiv : the preprint server for biology · 2025Article
- Nuclear receptor coregulator NRIP1 R448G modulates T cell gut homing to control intestinal inflammation.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Modulation of cardiac fatty acid or glucose oxidation to treat heart failure in preclinical models: a systematic review and meta-analysis.Communications medicine · 2025Article
- NRIP1 is a downstream target of YY1 in promoting OGD/R-induced H9c2 cardiomyocyte injury and mitochondrial dysfunction.Histology and histopathology · 2025Article
- Elucidating cardiomyocyte heterogeneity and maturation dynamics through integrated single-cell and spatial transcriptomics.iScience · 2025Article
- SIRT5 prevents mitochondrial dysfunction and cardiac hypertrophy induced by RIP140.Iranian journal of basic medical sciences · 2025Article
- Nuclear receptor-driven immunometabolic crosstalk: immune-centric pharmacology targeting the inflamed nexus.Frontiers in cell and developmental biology · 2025Review
- Oxidative Stress and the Nrf2/PPARγ Axis in the Endometrium: Insights into Female Fertility.Cells · 2024Review
- Cardiac maturation.Journal of molecular and cellular cardiology · 2024Review
Corrections and comments
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Authors and funding
18 authors at 3 institutions in 1 country.
Funding
Abstract
During the development of heart failure (HF), the capacity for cardiomyocyte (CM) fatty acid oxidation (FAO) and ATP production is progressively diminished, contributing to pathologic cardiac hypertrophy and contractile dysfunction. Receptor-interacting protein 140 (RIP140, encoded by Nrip1) has been shown to function as a transcriptional corepressor of oxidative metabolism. We found that mice with striated muscle deficiency of RIP140 (strNrip1-/-) exhibited increased expression of a broad array of genes involved in mitochondrial energy metabolism and contractile function in heart and skeletal muscle. strNrip1-/- mice were resistant to the development of pressure overload-induced cardiac hypertrophy, and CM-specific RIP140-deficient (csNrip1-/-) mice were protected against the development of HF caused by pressure overload combined with myocardial infarction. Genomic enhancers activated by RIP140 deficiency in CMs were enriched in binding motifs for transcriptional regulators of mitochondrial function (estrogen-related receptor) and cardiac contractile proteins (myocyte enhancer factor 2). Consistent with a role in the control of cardiac fatty acid oxidation, loss of RIP140 in heart resulted in augmented triacylglyceride turnover and fatty acid utilization. We conclude that RIP140 functions as a suppressor of a transcriptional regulatory network that controls cardiac fuel metabolism and contractile function, representing a potential therapeutic target for the treatment of HF.
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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.