@article{6c6d9b6af7df4ece8f10ed8526dcce3c,
title = "Transcription factors as therapeutic targets in chronic kidney disease",
abstract = "The growing number of patients with chronic kidney disease (CKD) is recognized as an emerging problem worldwide. Recent studies have indicated that deregulation of transcription factors is associated with the onset or progression of kidney disease. Several clinical trials indicated that regression of CKD may be feasible via activation of the transcription factor nuclear factor erythroid-2 related factor 2 (Nrf2), which suggests that transcription factors may be potential drug targets for CKD. Agents stabilizing hypoxia-inducible factor (HIF), which may be beneficial for renal anemia and renal protection, are also now under clinical trial. Recently, we have reported that the transcription factor Kruppel-like factor 4 (KLF4) regulates the glomerular podocyte epigenome, and that the antiproteinuric effect of the renin–angiotensin system blockade may be partially mediated by KLF4. KLF4 is one of the Yamanaka factors that induces iPS cells and is reported to be involved in epigenetic remodeling. In this article, we summarize the transcription factors associated with CKD and particularly focus on the possibility of transcription factors being novel drug targets for CKD through epigenetic modulation.",
keywords = "Bardoxolone methyl, Chronic kidney disease (CKD), HIF, KLF4, Nrf2, Renin–angiotensin system (RAS)",
author = "Akihito Hishikawa and Kaori Hayashi and Hiroshi Itoh",
note = "Funding Information: Acknowledgments: A.H. was supported by the Keio University Doctorate Student Grant-in-Aid Program and a Grant-in-Aid for JSPS Fellows (No. 201813428). K.H. was supported by Grants for Scientific Research (25860687 and 16K19496) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan; Keio University Research Grants for Life Science and Medicine; a grant from the Banyu Life Science Foundation International; Ishibashi Yukiko Memorial Foundation; Japan Medical Woman{\textquoteright}s Association; Japanese Association of Dialysis Physicians; Asahi Life foundation; Takeda Science Foundation; and Daiwa Securities Health Foundation, Tokyo, Japan. Funding Information: A.H. was supported by the Keio University Doctorate Student Grant-in-Aid Program and a Grant-in-Aid for JSPS Fellows (No. 201813428). K.H. was supported by Grants for Scientific Research (25860687 and 16K19496) from the Ministry of Education, Culture, Sports, Science and Technology (MEXT) of Japan; Keio University Research Grants for Life Science and Medicine; a grant from the Banyu Life Science Foundation International; Ishibashi Yukiko Memorial Foundation; Japan Medical Woman{\textquoteright}s Association; Japanese Association of Dialysis Physicians; Asahi Life foundation; Takeda Science Foundation; and Daiwa Securities Health Foundation, Tokyo, Japan. Publisher Copyright: {\textcopyright} 2018 by the authors.",
year = "2018",
doi = "10.3390/molecules23051123",
language = "English",
volume = "23",
journal = "Molecules",
issn = "1420-3049",
publisher = "Multidisciplinary Digital Publishing Institute (MDPI)",
number = "5",
}