Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition
Acute kidney injury (AKI) was previously thought to be a merely transient event; however, recent epidemiological evidence supports the existence of a causal relationship between AKI episodes and subsequent progression to chronic kidney disease (CKD). Although the pathophysiology of this AKI-to-CKD t...
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MDPI AG
2022-01-01
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Series: | Pharmaceuticals |
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Online Access: | https://www.mdpi.com/1424-8247/15/2/123 |
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author | Fumiaki Tanemoto Imari Mimura |
author_facet | Fumiaki Tanemoto Imari Mimura |
author_sort | Fumiaki Tanemoto |
collection | DOAJ |
description | Acute kidney injury (AKI) was previously thought to be a merely transient event; however, recent epidemiological evidence supports the existence of a causal relationship between AKI episodes and subsequent progression to chronic kidney disease (CKD). Although the pathophysiology of this AKI-to-CKD transition is not fully understood, it is mediated by the interplay among multiple components of the kidney including tubular epithelial cells, endothelial cells, pericytes, inflammatory cells, and myofibroblasts. Epigenetic alterations including histone modification, DNA methylation, non-coding RNAs, and chromatin conformational changes, are also expected to be largely involved in the pathophysiology as a “memory” of the initial injury that can persist and predispose to chronic progression of fibrosis. Each epigenetic modification has a great potential as a therapeutic target of AKI-to-CKD transition; timely and target-specific epigenetic interventions to the various temporal stages of AKI-to-CKD transition will be the key to future therapeutic applications in clinical practice. This review elaborates on the latest knowledge of each mechanism and the currently available therapeutic agents that target epigenetic modification in the context of AKI-to-CKD transition. Further studies will elucidate more detailed mechanisms and novel therapeutic targets of AKI-to-CKD transition. |
first_indexed | 2024-03-09T21:15:39Z |
format | Article |
id | doaj.art-1d314603b5e34d9d90b28c1fca4c6d23 |
institution | Directory Open Access Journal |
issn | 1424-8247 |
language | English |
last_indexed | 2024-03-09T21:15:39Z |
publishDate | 2022-01-01 |
publisher | MDPI AG |
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series | Pharmaceuticals |
spelling | doaj.art-1d314603b5e34d9d90b28c1fca4c6d232023-11-23T21:33:23ZengMDPI AGPharmaceuticals1424-82472022-01-0115212310.3390/ph15020123Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease TransitionFumiaki Tanemoto0Imari Mimura1Division of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine; Tokyo 113-0033, JapanDivision of Nephrology and Endocrinology, The University of Tokyo Graduate School of Medicine; Tokyo 113-0033, JapanAcute kidney injury (AKI) was previously thought to be a merely transient event; however, recent epidemiological evidence supports the existence of a causal relationship between AKI episodes and subsequent progression to chronic kidney disease (CKD). Although the pathophysiology of this AKI-to-CKD transition is not fully understood, it is mediated by the interplay among multiple components of the kidney including tubular epithelial cells, endothelial cells, pericytes, inflammatory cells, and myofibroblasts. Epigenetic alterations including histone modification, DNA methylation, non-coding RNAs, and chromatin conformational changes, are also expected to be largely involved in the pathophysiology as a “memory” of the initial injury that can persist and predispose to chronic progression of fibrosis. Each epigenetic modification has a great potential as a therapeutic target of AKI-to-CKD transition; timely and target-specific epigenetic interventions to the various temporal stages of AKI-to-CKD transition will be the key to future therapeutic applications in clinical practice. This review elaborates on the latest knowledge of each mechanism and the currently available therapeutic agents that target epigenetic modification in the context of AKI-to-CKD transition. Further studies will elucidate more detailed mechanisms and novel therapeutic targets of AKI-to-CKD transition.https://www.mdpi.com/1424-8247/15/2/123AKI-to-CKDacute kidney injurychronic kidney diseasehistonehypoxic memoryhistone acetylation |
spellingShingle | Fumiaki Tanemoto Imari Mimura Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition Pharmaceuticals AKI-to-CKD acute kidney injury chronic kidney disease histone hypoxic memory histone acetylation |
title | Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition |
title_full | Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition |
title_fullStr | Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition |
title_full_unstemmed | Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition |
title_short | Therapies Targeting Epigenetic Alterations in Acute Kidney Injury-to-Chronic Kidney Disease Transition |
title_sort | therapies targeting epigenetic alterations in acute kidney injury to chronic kidney disease transition |
topic | AKI-to-CKD acute kidney injury chronic kidney disease histone hypoxic memory histone acetylation |
url | https://www.mdpi.com/1424-8247/15/2/123 |
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