Abstract
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.
Highlights
Academic Editor: MarcinChronic kidney disease (CKD) is defined as persistent abnormalities of the kidney structure or renal function [1]
Undergoing polyploidization results in a predisposition to subsequent chronic kidney disease (CKD) [17]. This dynamic physiological repair mechanism following tubular injury explains the background pathology of Acute kidney injury (AKI)-to-CKD transition in part for moderate to severe AKI, this mechanism does not encompass all of the factors associated with Tubular epithelial cells (TECs) contributing to pathogenesis
3C assay, we found that hypoxia-inducible factor (HIF)-1, a master transcription factor hypoxia, and lysine-specific demethylase conjugately regulated the expresunder hypoxia, and lysine-specific demethylase conjugately regulated the sion of a down-stream targettarget gene,gene, solutesolute carrier family
Summary
Chronic kidney disease (CKD) is defined as persistent abnormalities of the kidney structure or renal function [1]. It is a very common condition caused by various kidney diseases with a reported prevalence of more than 10% worldwide [2]. In contrast to CKD, acute kidney injury (AKI) is defined as a sudden loss of renal function, which is a very common condition with high morbidity and mortality during the acute phase [7,8]. Animal studies indicate that maladaptive repair following recovery from AKI results in decreased kidney function and the development of renal fibrosis, which supports the existence of AKI-to-CKD transition [12,16]. The latest evidence for epigenetic modifications contributing to the pathogenesis of AKI-to-CKD transition and their potential role as novel therapeutic targets are discussed in detail
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