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Krüppel-like factor 15 (KLF15) is a member of the Krüppel-like factor family of transcription factors, characterized by Cys2His2 zinc finger motifs that allow it to bind specific DNA sequences and regulate the transcription of target genes[1][2][4]. It is highly expressed in liver, kidney, heart, and skeletal muscle and is regulated by hormones such as insulin and glucocorticoids[1]. KLF15 plays a crucial role in the regulation of metabolic pathways, especially gluconeogenesis, lipid metabolism, and adipogenesis; it is involved in both physiological (e.g., response to fasting, circadian variations) and pathophysiological (heart failure, fibrosis, metabolic disease) processes[1][2][3]. Therapeutically, KLF15 is considered a potential target for conditions such as cardiac remodeling, aortic disease, metabolic syndrome, and even certain cancers and viral infections[1][3]. Levels of KLF15 are influenced by multiple signals (insulin, glucocorticoids, progestins), and its genetic or pharmacological modulation has been associated with phenotypes ranging from altered insulin sensitivity and fat storage to cardiac hypertrophy and arrhythmia susceptibility[1][2][3][4].
Downregulation by drugs (e.g., metformin) leads to reduced expression of gluconeogenic genes[1].
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