ArticleCardiovascular research2015
Modulation of cardiac fibrosis by Krüppel-like factor 6 through transcriptional control of thrombospondin 4 in cardiomyocytes.
Article in Cardiovascular research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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25 citing papers in PubMed, 45 citations in OpenAlex.
- Decoding fibroblast activation: Transcriptional networks in hepatic stellate cells and across fibrotic organs (Review).International journal of molecular medicine · 2026Review
- THBS4 Regulates Pulmonary Hypertension via TGF-β/SMAD2 Signaling.Hypertension (Dallas, Tex. : 1979) · 2026Article
- DANSE: a pipeline for dynamic modelling of time-series multi-omics data.BMC bioinformatics · 2025Article
- Retrospective transcriptomic analysis indicates temporal dysregulation of mitochondrial genes and metabolic pathways after volumetric muscle loss injury.Physiological reports · 2025Article
- Podocyte-specific KLF6 primes proximal tubule CaMK1D signaling to attenuate diabetic kidney disease.Nature communications · 2024Article
- Suppression of RBFox2 by Multiple MiRNAs in Pressure Overload-Induced Heart Failure.International journal of molecular sciences · 2023Article
- A non-coding GWAS variant impacts anthracycline-induced cardiotoxic phenotypes in human iPSC-derived cardiomyocytes.Nature communications · 2022Article
- Asporin, an extracellular matrix protein, is a beneficial regulator of cardiac remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2022Article
- Single cell transcriptomics and TCR reconstruction reveal CD4 T cell response to MHC-II-restricted APOB epitope in human cardiovascular disease.Nature cardiovascular research · 2022Article
- A New Hypothetical Concept in Metabolic Understanding of Cardiac Fibrosis: Glycolysis Combined with TGF-β and KLF5 Signaling.International journal of molecular sciences · 2022Review
- Lack of food intake during shift work alters the heart transcriptome and leads to cardiac tissue fibrosis and inflammation in rats.BMC biology · 2022Article
- Krüppel-like factor (KLF)5: An emerging foe of cardiovascular health.Journal of molecular and cellular cardiology · 2022Review
- Krüppel-like factor 6-mediated loss of BCAA catabolism contributes to kidney injury in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Full-Length Transcriptome Sequencing: An Insight Into the Dog Model of Heart Failure.Frontiers in cardiovascular medicine · 2021Article
- Thrombospondin-4 induces prolongation of action potential duration in rat isolated ventricular myocytes.The Journal of veterinary medical science · 2020Article
- The Extracellular Matrix in Ischemic and Nonischemic Heart Failure.Circulation research · 2019Review
- Thrombospondin-4 in tissue remodeling.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Krüppel-like factors: Crippling and un-crippling metabolic pathways.JACC. Basic to translational science · 2018Article
- Overexpressed microRNA-506 and microRNA-124 alleviate H2O2-induced human cardiomyocyte dysfunction by targeting krüppel-like factor 4/5.Molecular medicine reports · 2017Article
- Editorial commentary: Endothelial-to-mesenchymal transition: When the good one goes bad.Trends in cardiovascular medicine · 2017Article
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16 authors at 8 institutions in 4 countries.
Funding
Abstract
aimsKrüppel-like factors (KLFs) are a family of transcription factors which play important roles in the heart under pathological and developmental conditions. We previously identified and cloned Klf6 whose homozygous mutation in mice results in embryonic lethality suggesting a role in cardiovascular development. Effects of KLF6 on pathological regulation of the heart were investigated in the present study. METHODS AND
resultsMice heterozygous for Klf6 resulted in significantly diminished levels of cardiac fibrosis in response to angiotensin II infusion. Intriguingly, a similar phenotype was seen in cardiomyocyte-specific Klf6 knockout mice, but not in cardiac fibroblast-specific knockout mice. Microarray analysis revealed increased levels of the extracellular matrix factor, thrombospondin 4 (TSP4), in the Klf6-ablated heart. Mechanistically, KLF6 directly suppressed Tsp4 expression levels, and cardiac TSP4 regulated the activation of cardiac fibroblasts to regulate cardiac fibrosis.
conclusionOur present studies on the cardiac function of KLF6 show a new mechanism whereby cardiomyocytes regulate cardiac fibrosis through transcriptional control of the extracellular matrix factor, TSP4, which, in turn, modulates activation of cardiac fibroblasts.
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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.