ArticlePloS one2018
Kruppel-like factor 15 is required for the cardiac adaptive response to fasting.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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
10 citing papers in PubMed, 12 citations in OpenAlex.
- Epigenetic and chromatin remodeling mechanisms across cardiomyopathies: a comprehensive review.Epigenetics & chromatin · 2026Review
- Effect ofInternational journal of molecular sciences · 2025Review
- KLF15 suppresses stemness of pancreatic cancer by decreasing USP21-mediated Nanog stability.Cellular and molecular life sciences : CMLS · 2024Article
- Deranged Myocardial Fatty Acid Metabolism in Heart Failure.International journal of molecular sciences · 2022Review
- Article
- KLF15 Regulates Oxidative Stress Response in Cardiomyocytes through NADMetabolites · 2021Article
- Molecular link between circadian clocks and cardiac function: a network of core clock, slave clock, and effectors.Current opinion in pharmacology · 2021Review
- Muscle Krüppel-like factor 15 regulates lipid flux and systemic metabolic homeostasis.The Journal of clinical investigation · 2021Article
- Article
- The Krüppel-Like Factors and Control of Energy Homeostasis.Endocrine reviews · 2019Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Cardiac metabolism is highly adaptive in response to changes in substrate availability, as occur during fasting. This metabolic flexibility is essential to the maintenance of contractile function and is under the control of a group of select transcriptional regulators, notably the nuclear receptor family of factors member PPARα. However, the diversity of physiologic and pathologic states through which the heart must sustain function suggests the possible existence of additional transcriptional regulators that play a role in matching cardiac metabolism to energetic demand. Here we show that cardiac KLF15 is required for the normal cardiac response to fasting. Specifically, we find that cardiac function is impaired upon fasting in systemic and cardiac specific Klf15-null mice. Further, cardiac specific Klf15-null mice display a fasting-dependent accumulation of long chain acylcarnitine species along with a decrease in expression of the carnitine translocase Slc25a20. Treatment with a diet high in short chain fatty acids relieves the KLF15-dependent long chain acylcarnitine accumulation and impaired cardiac function in response to fasting. Our observations establish KLF15 as a critical mediator of the cardiac adaptive response to fasting through its regulation of myocardial lipid utilization.
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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.