Roles of Krüppel‐like factor 5 in kidney disease

• Published in: Journal of cellular and molecular medicine Vol. 25; no. 5; pp. 2342 - 2355
• Main Authors: Li, Jia, Liu, Liang, Zhou, Wen‐Qian, Cai, Lu, Xu, Zhong‐Gao, Rane, Madhavi J.
• Format: Journal Article
• Language: English
• Published: England John Wiley & Sons, Inc 01-03-2021; John Wiley and Sons Inc
• Subjects: Amino acids; Animal models; Apoptosis; Cardiovascular diseases; Cell culture; Cell growth; Cell proliferation; Chromosomes; Clonal deletion; Colon; Cyclin-dependent kinases; Deoxyribonucleic acid; diabetes; DNA; DNA methylation; Fibrosis; Gastrointestinal diseases; Gene deletion; Gene expression; Inflammation; kidney disease; Kidney diseases; Kinases; Krüppel‐like factor 5; Krüppel‐like factors; Lipids; Localization; Metabolism; MicroRNAs; Pathogenesis; Phosphorylation; Protein expression; Proteins; Review; Reviews; Small intestine; Transcription factors; Krüppel-like factor 5; kidney disease; fibrosis; inflammation; diabetes; Krüppel-like factors
• ISSN: 1582-1838; 1582-4934
• DOI: 10.1111/jcmm.16332

Transcription factor Krüppel‐like factor 5 (KLF5) is a member of the Krüppel‐like factors’ (KLFs) family. KLF5 regulates a number of cellular functions, such as apoptosis, proliferation and differentiation. Therefore, KLF5 can play a role in many diseases, including, cancer, cardiovascular disease and gastrointestinal disorders. An important role for KLF5 in the kidney was recently reported, such that KLF5 regulated podocyte apoptosis, renal cell proliferation, tubulointerstitial inflammation and renal fibrosis. In this review, we have summarized the available information in the literature with a brief description on how transcriptional, post‐transcriptional and post‐translational modifications of KLF5 modulate its function in a variety of organs including the kidney with a focus of its importance on the pathogenesis of various kidney diseases. Furthermore, we also have outlined the current and possible mechanisms of KLF5 activation in kidney diseases. These studies suggest a need for more systemic investigations, particularly for generation of animal models with renal cell‐specific deletion or overexpression of KLF5 gene to examine direct contributions of KLF5 to various kidney diseases. This will promote further experimentation in the development of therapies to prevent or treat various kidney diseases.