Abstract
The incidence of chronic kidney disease (CKD) has rapidly increased in the past decades. A progressive loss of kidney function characterizes a part of CKD even with intensive supportive treatment. Irrespective of its etiology, CKD progression is generally accompanied with the development of chronic kidney inflammation that is pathologically featured by the low-grade but chronic activation of recruited immune cells. Cumulative evidence support that aberrant DNA methylation pattern of diverse peripheral immune cells, including T cells and monocytes, is closely associated with CKD development in many chronic disease settings. The change of DNA methylation profile can sustain for a long time and affect the future genes expression in the circulating immune cells even after they migrate from the circulation into the involved kidney. It is of clinical interest to reveal the underlying mechanism of how altered DNA methylation regulates the intensity and the time length of the inflammatory response in the recruited effector cells. We and others recently demonstrated that altered DNA methylation occurs in peripheral immune cells and profoundly contributes to CKD development in systemic chronic diseases, such as diabetes and hypertension. This review will summarize the current findings about the influence of aberrant DNA methylation on circulating immune cells and how it potentially determines the outcome of CKD.
Highlights
Over the past decades, the incidence of chronic kidney disease (CKD) has rapidly increased worldwide (GBD Chronic Kidney Disease Collaboration, 2020), likely due to the huge changes in human living habits and the environment
Rasal1 methylation, which is dependent on Tet3-mediated hydroxymethylation
It remains necessary to clarify the causal relationship between DNA methylation and CKD development, since it is technically hard to separate “driver” events from “passenger” events in the setting of SCI
Summary
The incidence of chronic kidney disease (CKD) has rapidly increased worldwide (GBD Chronic Kidney Disease Collaboration, 2020), likely due to the huge changes in human living habits and the environment. Rasal1 methylation, which is dependent on Tet3-mediated hydroxymethylation Mouse streptozotocin -induced DKD, mouse UUO, COL4A3-deficient Alport mice, mouse 5/6 nephrectomy-induced CKD Mouse UUO Mouse MRL/lpr lupus Fibrosis↓ Renal function↑, proteinuria↓, Renal injury↓ Fibrosis↓
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