New insights into molecular mechanisms of epigenetic regulation in kidney disease
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- Imari Mimura
- Division of Nephrology and Endocrinology The University of Tokyo Tokyo Japan
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- Tetsuhiro Tanaka
- Division of Nephrology and Endocrinology The University of Tokyo Tokyo Japan
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- Masaomi Nangaku
- Division of Nephrology and Endocrinology The University of Tokyo Tokyo Japan
書誌事項
- 公開日
- 2016-11-21
- 資源種別
- journal article
- 権利情報
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- http://onlinelibrary.wiley.com/termsAndConditions#vor
- DOI
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- 10.1111/1440-1681.12663
- 公開者
- Wiley
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説明
<jats:title>Summary</jats:title><jats:p>The number of patients with kidney failure has increased in recent years. Different factors contribute to the progression of chronic kidney disease, including glomerular sclerosis, atherosclerosis of the renal arteries and tubulointerstitial fibrosis. Tubulointerstitial injury is induced by hypoxia and other inflammatory signals, leading to fibroblast activation. Technological advances using high‐throughput sequencing has enabled the determination of the expression profile of almost all genes, revealing that gene expression is intricately regulated by <jats:styled-content style="fixed-case">DNA</jats:styled-content> methylation, histone modification, changes in chromosome conformation, long non‐coding <jats:styled-content style="fixed-case">RNA</jats:styled-content>s and micro<jats:styled-content style="fixed-case">RNA</jats:styled-content>s. These epigenetic modifications are stored as cellular epigenetic memory. Epigenetic memory leads to adult‐onset disease or ageing in the long term and may possibly play an important role in the kidney disease process. Herein we emphasize the importance of clarifying the molecular mechanisms underlying epigenetic modifications because this may lead to the development of new therapeutic targets in kidney disease.</jats:p>
収録刊行物
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- Clinical and Experimental Pharmacology and Physiology
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Clinical and Experimental Pharmacology and Physiology 43 (12), 1159-1167, 2016-11-21
Wiley