ArticleProceedings of the National Academy of Sciences of the United States of America2007
Kruppel-like factor 15 is a regulator of cardiomyocyte hypertrophy.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 115 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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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
115 citing papers in PubMed, 214 citations in OpenAlex.
- FoxO transcription factors coordinate the urea cycle and gluconeogenesis by controllingiScience · 2026Article
- Cardiomyocyte-Specific Smad7 Protects the Pressure-Overloaded Heart, Inhibiting the Transforming Growth Factor-β Receptor 1/Smad2/3 Cascade.Journal of the American Heart Association · 2026Article
- Enhancing KLF15 activity in cardiomyocytes: a novel approach to prevent pathological reprogramming and fibrosis via nuclease-deficient dCas9VPR.Signal transduction and targeted therapy · 2026Article
- A reduced TBX5-dependent gene regulatory network links atrial fibrillation and heart failure.Nature cardiovascular research · 2026Article
- Unraveling the Bone-Brain Communication Network.Biology · 2025Review
- Acute HSV-1 Ocular Infection Is Impaired in KLF15 Knockout Mice but Stress-Induced Reactivation from Latency Is Prolonged in Male KLF15 Knockout Mice.Pathogens (Basel, Switzerland) · 2025Article
- KLF9 aggravates the cardiomyocyte hypertrophy in hypertrophic obstructive cardiomyopathy through the lncRNA UCA1/p27 axis.International journal of experimental pathology · 2025Article
- Computational analysis of congenital heart disease associated SNPs: unveiling their impact on the gene regulatory system.BMC genomics · 2025Article
- Multi-omics insights into the pathogenesis of diabetic cardiomyopathy: epigenetic and metabolic profiles.Epigenomics · 2025Article
- In recent research: exosomal and molecular regulators of browning and thermogenesis in adipose tissues.Turkish journal of medical sciences · 2025Review
- Primary Roles of Branched Chain Amino Acids (BCAAs) and Their Metabolism in Physiology and Metabolic Disorders.Molecules (Basel, Switzerland) · 2024Review
- Glucocorticoid chronopharmacology promotes glucose metabolism in heart through a cardiomyocyte-autonomous transactivation program.JCI insight · 2024Article
- Klf9 is essential for cardiac mitochondrial homeostasis.Nature cardiovascular research · 2024Article
- Glucocorticoid chrono-pharmacology unveils novel targets for the cardiomyocyte-specific GR-KLF15 axis in cardiac glucose metabolism.bioRxiv : the preprint server for biology · 2024Article
- Effects of Halloysite Nanotubes and Multi-walled Carbon Nanotubes on Kruppel-like Factor 15-Mediated Downstream Events in Mouse Hearts After Intravenous Injection.Cardiovascular toxicology · 2024Article
- Krüpple-like factors in cardiomyopathy: emerging player and therapeutic opportunities.Frontiers in cardiovascular medicine · 2024Review
- Klf9 plays a critical role in GR -dependent metabolic adaptations in cardiomyocytes.Cellular signalling · 2023Article
- Giant mitochondria in cardiomyocytes: cellular architecture in health and disease.Basic research in cardiology · 2023Review
- Dietary essential amino acids for the treatment of heart failure with reduced ejection fraction.Cardiovascular research · 2023Article
- A defect in mitochondrial protein translation influences mitonuclear communication in the heart.Nature communications · 2023Article
55 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issuedPinto, Yigal [corrected to Pinto, Yigal M]
Authors and funding
19 authors at 7 institutions in 2 countries.
Funding
Abstract
Cardiac hypertrophy is a common response to injury and hemodynamic stress and an important harbinger of heart failure and death. Herein, we identify the Kruppel-like factor 15 (KLF15) as an inhibitor of cardiac hypertrophy. Myocardial expression of KLF15 is reduced in rodent models of hypertrophy and in biopsy samples from patients with pressure-overload induced by chronic valvular aortic stenosis. Overexpression of KLF15 in neonatal rat ventricular cardiomyocytes inhibits cell size, protein synthesis and hypertrophic gene expression. KLF15-null mice are viable but, in response to pressure overload, develop an eccentric form of cardiac hypertrophy characterized by increased heart weight, exaggerated expression of hypertrophic genes, left ventricular cavity dilatation with increased myocyte size, and reduced left ventricular systolic function. Mechanistically, a combination of promoter analyses and gel-shift studies suggest that KLF15 can inhibit GATA4 and myocyte enhancer factor 2 function. These studies identify KLF15 as part of a heretofore unrecognized pathway regulating the cardiac response to hemodynamic stress.
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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.