Epigenetics in acute kidney injury

Tang, Jinhua; Zhuang, Songlin

doi:10.1097/mnh.0000000000000140

Cited by 48 publications

(59 citation statements)

References 68 publications

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“…A new development in AKI research is the recognition of the involvement of epigenetic regulation in kidney injury and subsequent recovery or repair (Tang, Dong, 2015; Tang, Zhuang, 2015). Epigenetics refers to heritable mechanisms that alter gene expression without changing DNA sequence.…”

Section: Agents Targeting Gene Expressionmentioning

confidence: 99%

Renoprotective approaches and strategies in acute kidney injury

Yang

Song

et al. 2016

Pharmacology & Therapeutics

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Acute kidney injury (AKI) is a major renal disease associated with a high mortality rate and increasing prevalence. Decades of research has suggested numerous chemical and biological agents with beneficial effects in AKI. In addition, cell therapy and molecular targeting have been explored for reducing kidney tissue damage and promoting kidney repair or recovery from AKI. Mechanistically, these approaches may mitigate oxidative stress, inflammation, cell death, and mitochondrial and other organellar damage, or activate cytoprotective mechanisms such as autophagy and pro-survival factors. However, none of these findings has been successfully translated into clinical treatment of AKI. In this review, we analyze these findings and propose experimental strategies for the identification of renoprotective agents or methods with clinical potential. Moreover, we propose the consideration of combination therapy by targeting multiple targets in AKI.

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Section: Agents Targeting Gene Expressionmentioning

confidence: 99%

Renoprotective approaches and strategies in acute kidney injury

Yang

Song

et al. 2016

Pharmacology & Therapeutics

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“…1). Recently, considerable attention has been paid to the role of epigenetic mechanisms and factors implied in cellular and subcellular responses associated with acute kidney injury, chronic kidney disease (CKD), heart failure and cardiovascular disease [20,21,22,23,24,25,26,27,28,29,30,31]. It is known that DNA methylation and histone modifications closely interact to control gene expression, and they may have a role in the organ cross talk [32,33].…”

Section: Epigenetics and Prenatal Programming In Crsmentioning

confidence: 99%

Molecular and Genetic Mechanisms Involved in the Pathogenesis of Cardiorenal Cross Talk

Virzì

Clementi²,

Brocca³

et al. 2016

Pathobiology

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The term ‘cardiorenal syndrome' (CRS) encloses a scenario of clinical interactions in which cardiac and renal dysfunctions coexist. The cross talk between the heart and the kidney is clearly evidenced but not fully understood. Indeed, different factors have been shown to be involved in the pathogenesis of CRS, such as systemic inflammation, oxidative stress, apoptosis and immune dysregulation. Recently, considerable attention has been paid to the role of new alternative mechanisms which may be implicated in the pathogenesis of cardiorenal cross talk. In this review, we will focus on epigenetics, prenatal programming, small noncoding RNAs and extracellular vesicles, aiming to elucidate their possible role in heart and kidney diseases.

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“…Such relaxation can be counteracted by histone deacetylase (HDAC) activity. Acetylation and deacetylation are typically catalyzed by two groups of enzymes: histone acetyltransferases (HAT) and HDAC . HAT are enzymes that acetylate lysine amino acids of histone proteins by transferring an acetyl group from acetyl CoA to form ε‐N‐acetyllysine.…”

mentioning

confidence: 99%

“…HAT are enzymes that acetylate lysine amino acids of histone proteins by transferring an acetyl group from acetyl CoA to form ε‐N‐acetyllysine. Whereas HDAC are a group of deacetylating enzymes that remove acetyl groups from ε‐amino groups of lysine residues of histones as well as non‐histones, causing the condensation of chromatin structure, and thereby repressing gene expression . There are four classes of HDAC: class I HDAC (HDAC1, 2, 3 and 8); class II HDAC (HDAC 4, 5, 6, 7, 9 and 10); class III (SIRT1–7); class IV (HDAC 11).…”

mentioning

confidence: 99%

Epigenetic targeting for acute kidney injury

Zhuang

2018

Nephrology

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In recent years, epigenetics has emerged as important mechanisms for the regulation of pathogenesis in many diseases, including acute kidney injury (AKI). Numerous studies have demonstrated that AKI is associated with the changes in epigenetics, including histone modifications, DNA methylation and the expression of various non‐coding RNAs. Through utilizing histone deacetylase (HDAC) inhibitors, studies have demonstrated that increase of histone acetylation either protects kidney from injury or potentiates this process, depending on which HDAC (s) isform is suppressed, whereas inhibition of histone methyltransferase, generally provides a protective effect in AKI. Although AKI is also associated with changes in DNA methylation, the role of DNA methylation in kidney injury remains unclear. In this article, we discuss the role and mechanism of histone acetylation and methylation in the pathogenesis of AKI.

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Epigenetics in acute kidney injury

Cited by 48 publications

References 68 publications

Renoprotective approaches and strategies in acute kidney injury

Renoprotective approaches and strategies in acute kidney injury

Molecular and Genetic Mechanisms Involved in the Pathogenesis of Cardiorenal Cross Talk

Epigenetic targeting for acute kidney injury

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