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Epigenetic Regulation in Chronic Kidney Disease and Its Complication

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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Genetics and Genomics".

Deadline for manuscript submissions: closed (31 August 2022) | Viewed by 8277

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Special Issue Editor

Prof. Dr. Tadashi Yoshida

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Guest Editor

Apheresis and Dialysis Center, Keio University School of Medicine, Tokyo, Japan
Interests: smooth muscle cells; vascular biology; vascular calcification; transcription factors; epigenetics; end-stage renal disease

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is defined by a reduced glomerular filtration rate, increased proteinuria, or both. The prevalence of CKD is estimated to be 8–16% worldwide. Patients with CKD are accompanied by a variety of complications, including anemia, hyperkalemia, hypocalcemia, hyperphosphatemia, secondary hyperparathyroidism, metabolic acidosis, and bone abnormalities. In addition, they are at high risk of cardiovascular disease and death. Thus far, therapeutic approaches to control these abnormal conditions have not been well developed yet. Recently, studies in the field of epigenetics have made significant progress. It has been realized that various epigenetic mechanisms, such as histone modifications, DNA methylation, ubiquitination, microRNAs, noncoding RNAs, etc. play crucial roles in the pathogenesis of multiple disease conditions, including CKD. In this Special Issue of the International Journal of Molecular Sciences, I would like to invite contributions addressing molecular and/or epigenetic mechanisms for the pathogenesis of CKD and its complications. Submissions can be either original research papers or reviews. Your contributions will be highly appreciated.

Prof. Dr. Tadashi Yoshida
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

chronic kidney disease
transcription
histone modification
DNA methylation
anemia
vascular calcification
calcium
phosphorus
dialysis

Published Papers (3 papers)

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Research

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16 pages, 2868 KiB

Open AccessArticle

Sirtuin 7 Deficiency Reduces Inflammation and Tubular Damage Induced by an Episode of Acute Kidney Injury

by Andrea Sánchez-Navarro, Miguel Ángel Martínez-Rojas, Adrián Albarrán-Godinez, Rosalba Pérez-Villalva, Johan Auwerx, Abigail de la Cruz, Lilia G. Noriega, Florencia Rosetti and Norma A. Bobadilla

Int. J. Mol. Sci. 2022, 23(5), 2573; https://doi.org/10.3390/ijms23052573 - 25 Feb 2022

Cited by 13 | Viewed by 2591

Abstract

Acute kidney injury (AKI) is a public health problem worldwide. Sirtuins are a family of seven NAD+-dependent deacylases, Overexpression of Sirtuin 1, 3, and 5 protect against AKI. However, the role of Sirtuin 7 (Sirt7) in AKI is not known. Here, we analyzed how Sirt7 deficient mice (KO-Sirt7) were affected by AKI. As expected, wild-type and Sirt7 heterozygotes mice that underwent renal ischemia/reperfusion (IR) exhibited the characteristic hallmarks of AKI: renal dysfunction, tubular damage, albuminuria, increased oxidative stress, and renal inflammation. In contrast, the KO-Sirt7+IR mice were protected from AKI, exhibiting lesser albuminuria and reduction in urinary biomarkers of tubular damage, despite similar renal dysfunction. The renoprotection in the Sirt7-KO+IR group was associated with reduced kidney weight, minor expression of inflammatory cytokines and less renal infiltration of inflammatory cells. This anti-inflammatory effect was related to diminished p65 expression and in its active phosphorylation, as well as by a reduction in p65 nuclear translocation. Sirt7 deficient mice are protected from AKI, suggesting that this histone deacetylase promotes tubular damage and renal inflammation. Therefore, our findings indicate that Sirt7 inhibitors may be an attractive therapeutic target to reduce NFκB signaling. Full article

(This article belongs to the Special Issue Epigenetic Regulation in Chronic Kidney Disease and Its Complication)

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Review

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16 pages, 736 KiB

Open AccessReview

Are Alterations in DNA Methylation Related to CKD Development?

by Jacek Rysz, Beata Franczyk, Magdalena Rysz-Górzyńska and Anna Gluba-Brzózka

Int. J. Mol. Sci. 2022, 23(13), 7108; https://doi.org/10.3390/ijms23137108 - 26 Jun 2022

Cited by 4 | Viewed by 2522

Abstract

The modifications in genomic DNA methylation are involved in the regulation of normal and pathological cellular processes. The epigenetic regulation stimulates biological plasticity as an adaptive response to variations in environmental factors. The role of epigenetic changes is vital for the development of some diseases, including atherogenesis, cancers, and chronic kidney disease (CKD). The results of studies presented in this review have suggested that altered DNA methylation can modulate the expression of pro-inflammatory and pro-fibrotic genes, as well those essential for kidney development and function, thus stimulating renal disease progression. Abnormally increased homocysteine, hypoxia, and inflammation have been suggested to alter epigenetic regulation of gene expression in CKD. Studies of renal samples have demonstrated the relationship between variations in DNA methylation and fibrosis and variations in estimated glomerular filtration rate (eGFR) in human CKD. The unravelling of the genetic–epigenetic profile would enhance our understanding of processes underlying the development of CKD. The understanding of multifaceted relationship between DNA methylation, genes expression, and disease development and progression could improve the ability to identify individuals at risk of CKD and enable the choice of appropriate disease management. Full article

(This article belongs to the Special Issue Epigenetic Regulation in Chronic Kidney Disease and Its Complication)

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20 pages, 6324 KiB

Open AccessReview

The Dynamics and Plasticity of Epigenetics in Diabetic Kidney Disease: Therapeutic Applications Vis-à-Vis

by Feng-Chih Kuo, Chia-Ter Chao and Shih-Hua Lin

Int. J. Mol. Sci. 2022, 23(2), 843; https://doi.org/10.3390/ijms23020843 - 13 Jan 2022

Cited by 8 | Viewed by 2568

Abstract

Chronic kidney disease (CKD) refers to the phenomenon of progressive decline in the glomerular filtration rate accompanied by adverse consequences, including fluid retention, electrolyte imbalance, and an increased cardiovascular risk compared to those with normal renal function. The triggers for the irreversible renal function deterioration are multifactorial, and diabetes mellitus serves as a major contributor to the development of CKD, namely diabetic kidney disease (DKD). Recently, epigenetic dysregulation emerged as a pivotal player steering the progression of DKD, partly resulting from hyperglycemia-associated metabolic disturbances, rising oxidative stress, and/or uncontrolled inflammation. In this review, we describe the major epigenetic molecular mechanisms, followed by summarizing current understandings of the epigenetic alterations pertaining to DKD. We highlight the epigenetic regulatory processes involved in several crucial renal cell types: Mesangial cells, podocytes, tubular epithelia, and glomerular endothelial cells. Finally, we highlight epigenetic biomarkers and related therapeutic candidates that hold promising potential for the early detection of DKD and the amelioration of its progression. Full article

(This article belongs to the Special Issue Epigenetic Regulation in Chronic Kidney Disease and Its Complication)

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