Longitudinal genome-wide DNA methylation changes in response to kidney failure replacement therapy

Witasp, Anna; Luttropp, Karin; Qureshi, Abdul Rashid; Bárány, Peter; Heimbürger, Olof; Wennberg, Lars; Ekström, Tomas J.; Shiels, Paul G.; Stenvinkel, Peter; Nordfors, Louise

doi:10.1038/s41598-021-04321-5

Cited by 11 publications

(11 citation statements)

References 98 publications

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“…A most recent study compared epigenome-wide methylation modification between healthy patients and renal failure replacement therapy patient (dialysis and kidney transplantation) at baseline (right before renal failure replacement therapy) and over 12 months treatment, they found that uremic milieu drives genome-wide methylation changes but partially reversed with kidney failure replacement therapy. However, 413 CpG sites remained differentially methylated at follow-up in renal replacement therapy, which merit further investigation (40). These observations suggest a role of DNA methylation in chronic inflammation, IF/TA and chronic allograft dysfunction in kidney transplantation.…”

Section: Chronic Rejection and Interstitial Fibrosis/ Tubular Atrophymentioning

confidence: 86%

Epigenetic Regulation in Kidney Transplantation

et al. 2022

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Kidney transplantation is a standard care for end stage renal disease, but it is also associated with a complex pathogenesis including ischemia-reperfusion injury, inflammation, and development of fibrosis. Over the past decade, accumulating evidence has suggested a role of epigenetic regulation in kidney transplantation, involving DNA methylation, histone modification, and various kinds of non-coding RNAs. Here, we analyze these recent studies supporting the role of epigenetic regulation in different pathological processes of kidney transplantation, i.e., ischemia-reperfusion injury, acute rejection, and chronic graft pathologies including renal interstitial fibrosis. Further investigation of epigenetic alterations, their pathological roles and underlying mechanisms in kidney transplantation may lead to new strategies for the discovery of novel diagnostic biomarkers and therapeutic interventions.

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Section: Chronic Rejection and Interstitial Fibrosis/ Tubular Atrophymentioning

confidence: 86%

Epigenetic Regulation in Kidney Transplantation

et al. 2022

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“…These authors also noted distinct localisation patterns for differentially methylated CpG sites for dialysis and transplant patients, and highlighted that the methylation status of regions associated with cellular aging or metabolism were particularly altered 12 months post-treatment, to become more in line with healthy control participants (139). 413 differentially methylated genes present in both dialysis and transplant patients remained unaltered 12 months post-treatment, identifying potentially distinct and robust CKD markers warranting future study (139).…”

Section: Epigenetic Modifications Provide An Additional Layer Of Vari...mentioning

confidence: 98%

Harnessing the Full Potential of Multi-Omic Analyses to Advance the Study and Treatment of Chronic Kidney Disease

Hill¹,

Ávila-Palència²,

Maxwell³

et al. 2022

Front. Nephrol.

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Chronic kidney disease (CKD) was the 12th leading cause of death globally in 2017 with the prevalence of CKD estimated at ~9%. Early detection and intervention for CKD may improve patient outcomes, but standard testing approaches even in developed countries do not facilitate identification of patients at high risk of developing CKD, nor those progressing to end-stage kidney disease (ESKD). Recent advances in CKD research are moving towards a more personalised approach for CKD. Heritability for CKD ranges from 30% to 75%, yet identified genetic risk factors account for only a small proportion of the inherited contribution to CKD. More in depth analysis of genomic sequencing data in large cohorts is revealing new genetic risk factors for common diagnoses of CKD and providing novel diagnoses for rare forms of CKD. Multi-omic approaches are now being harnessed to improve our understanding of CKD and explain some of the so-called ‘missing heritability’. The most common omic analyses employed for CKD are genomics, epigenomics, transcriptomics, metabolomics, proteomics and phenomics. While each of these omics have been reviewed individually, considering integrated multi-omic analysis offers considerable scope to improve our understanding and treatment of CKD. This narrative review summarises current understanding of multi-omic research alongside recent experimental and analytical approaches, discusses current challenges and future perspectives, and offers new insights for CKD.

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“…Existing evidence suggests that DNA methylation plays a crucial role in the pathogenesis of kidney diseases (Chen et al, 2021; Witasp et al, 2022). Changes in DNA methylation can modify mitochondrial functions by either upregulating or suppressing the genes responsible for cellular processes such as an increase in ROS generation and alteration in energy metabolism (Lopes, 2020).…”

Section: Mitochondrial Dynamics In Kidney Diseasesmentioning

confidence: 99%

Epigenetic regulation of mitochondrial‐endoplasmic reticulum dynamics in kidney diseases

Shelke,

Yelgonde,

Kale

et al. 2023

Journal Cellular Physiology

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Kidney diseases are serious health problems affecting >800 million individuals worldwide. The high number of affected individuals and the severe consequences of kidney dysfunction demand an intensified effort toward more effective prevention and treatment. The pathophysiology of kidney diseases is complex and comprises diverse organelle dysfunctions including mitochondria and endoplasmic reticulum (ER). The recent findings prove interactions between the ER membrane and nearly all cell compartments and give new insights into molecular events involved in cellular mechanisms in health and disease. Interactions between the ER and mitochondrial membranes, known as the mitochondria‐ER contacts regulate kidney physiology by interacting with each other via membrane contact sites (MCS). ER controls mitochondrial dynamics through ER stress sensor proteins or by direct communication via mitochondria‐associated ER membrane to activate signaling pathways such as apoptosis, calcium transport, and autophagy. More importantly, these organelle dynamics are found to be regulated by several epigenetic mechanisms such as DNA methylation, histone modifications, and noncoding RNAs and can be a potential therapeutic target against kidney diseases. However, a thorough understanding of the role of epigenetic regulation of organelle dynamics and their functions is not well understood. Therefore, this review will unveil the role of epigenetic mechanisms in regulating organelle dynamics during various types of kidney diseases. Moreover, we will also shed light on different stress origins in organelles leading to kidney disease. Henceforth, by understanding this we can target epigenetic mechanisms to maintain/control organelle dynamics and serve them as a novel therapeutic approach against kidney diseases.

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Longitudinal genome-wide DNA methylation changes in response to kidney failure replacement therapy

Cited by 11 publications

References 98 publications

Epigenetic Regulation in Kidney Transplantation

Epigenetic Regulation in Kidney Transplantation

Harnessing the Full Potential of Multi-Omic Analyses to Advance the Study and Treatment of Chronic Kidney Disease

Epigenetic regulation of mitochondrial‐endoplasmic reticulum dynamics in kidney diseases

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