ArticleThe Journal of biological chemistry2010
Regulation of cardiac gene expression by KLF15, a repressor of myocardin activity.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 64 citations in OpenAlex.
- Article
- 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
- Role of branched chain amino acid metabolism on aging.Biogerontology · 2025Review
- Prognostic value of KLFs family genes in renal clear cell carcinoma.Scientific reports · 2024Article
- Krüpple-like factors in cardiomyopathy: emerging player and therapeutic opportunities.Frontiers in cardiovascular medicine · 2024Review
- The Involvement of Krüppel-like Factors in Cardiovascular Diseases.Life (Basel, Switzerland) · 2023Review
- Branched-chain amino acids in cardiovascular disease.Nature reviews. Cardiology · 2023Review
- CTRP12 alleviates cardiomyocyte ischemia‑reperfusion injury via regulation of KLF15.Molecular medicine reports · 2022Article
- Article
- Glucose-6-phosphate dehydrogenase and MEG3 controls hypoxia-induced expression of serum response factor (SRF) and SRF-dependent genes in pulmonary smooth muscle cell.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2022Article
- Stem cell-derived extracellular vesicles reduce the expression of molecules involved in cardiac hypertrophy-In a model of human-induced pluripotent stem cell-derived cardiomyocytes.Frontiers in pharmacology · 2022Article
- PA and OA induce abnormal glucose metabolism by inhibiting KLF15 in adipocytes.Nutrition & metabolism · 2021Article
- Is branched-chain amino acid nutritional supplementation beneficial or detrimental in heart failure?World journal of cardiology · 2021Review
- Obestatin signalling counteracts glucocorticoid-induced skeletal muscle atrophy via NEDD4/KLF15 axis.Journal of cachexia, sarcopenia and muscle · 2021Article
- FoxO1-Dio2 signaling axis governs cardiomyocyte thyroid hormone metabolism and hypertrophic growth.Nature communications · 2020Article
- Impaired branched chain amino acid oxidation contributes to cardiac insulin resistance in heart failure.Cardiovascular diabetology · 2019Article
- Targeting the glucagon receptor improves cardiac function and enhances insulin sensitivity following a myocardial infarction.Cardiovascular diabetology · 2019Article
- Estrogen receptor beta maintains expression of KLF15 to prevent cardiac myocyte hypertrophy in female rodents.Molecular and cellular endocrinology · 2018Article
- Left ventricular hypertrophy in experimental chronic kidney disease is associated with reduced expression of cardiac Kruppel-like factor 15.BMC nephrology · 2018Article
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pathological forms of left ventricular hypertrophy (LVH) often progress to heart failure. Specific transcription factors have been identified that activate the gene program to induce pathological forms of LVH. It is likely that apart from activating transcriptional inducers of LVH, constitutive transcriptional repressors need to be removed during the development of cardiac hypertrophy. Here, we report that the constitutive presence of Krüppel-like factor 15 (KLF15) is lost in pathological hypertrophy and that this loss precedes progression toward heart failure. We show that transforming growth factor-beta-mediated activation of p38 MAPK is necessary and sufficient to decrease KLF15 expression. We further show that KLF15 robustly inhibits myocardin, a potent transcriptional activator. Loss of KLF15 during pathological LVH relieves the inhibitory effects on myocardin and stimulates the expression of serum response factor target genes, such as atrial natriuretic factor. This uncovers a novel mechanism where activated p38 MAPK decreases KLF15, an important constitutive transcriptional repressor whose removal seems a vital step to allow the induction of pathological LVH.
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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.