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Review
. 2022 May 12:9:736006.
doi: 10.3389/fmed.2022.736006. eCollection 2022.

Protein Methylation in Diabetic Kidney Disease

Affiliations
Review

Protein Methylation in Diabetic Kidney Disease

Ye Cheng et al. Front Med (Lausanne). .

Abstract

Chronic kidney disease (CKD) is defined by persistent urine aberrations, structural abnormalities, or impaired excretory renal function. Diabetes is the leading cause of CKD. Their common pathological manifestation is renal fibrosis. Approximately half of all patients with type 2 diabetes and one-third with type 1 diabetes will develop CKD. However, renal fibrosis mechanisms are still poorly understood, especially post-transcriptional and epigenetic regulation. And an unmet need remains for innovative treatment strategies for preventing, arresting, treating, and reversing diabetic kidney disease (DKD). People believe that protein methylation, including histone and non-histone, is an essential type of post-translational modification (PTM). However, prevalent reviews mainly focus on the causes such as DNA methylation. This review will take insights into the protein part. Furthermore, by emphasizing the close relationship between protein methylation and DKD, we will summarize the clinical research status and foresee the application prospect of protein methyltransferase (PMT) inhibitors in DKD treatment. In a nutshell, our review will contribute to a more profound understanding of DKD's molecular mechanism and inspire people to dig into this field.

Keywords: chronic kidney disease; histone methylation; nonhistone methylation; protein methylation; renal fibrosis.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
(A–C) Diverse protein methylation.
FIGURE 2
FIGURE 2
Histone lysine methylation in DKD.
FIGURE 3
FIGURE 3
Functional mechanism of protein methyltransferase inhibitors.

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References

    1. Coresh J, Selvin E, Stevens LA, Manzi J, Kusek JW, Eggers P, et al. Prevalence of chronic kidney disease in the United States. JAMA. (2007) 298:2038–47. - PubMed
    1. Hsu C-Y, Vittinghoff E, Lin F, Shlipak MG. The incidence of end-stage renal disease is increasing faster than the prevalence of chronic renal insufficiency. Ann Intern Med. (2004) 141:95–101. 10.7326/0003-4819-141-2-200407200-00007 - DOI - PubMed
    1. Plantinga LC, Boulware LE, Coresh J, Stevens LA, Miller ER, Saran R, et al. Patient awareness of chronic kidney disease: trends and predictors. Arch Intern Med. (2008) 168:2268–75. 10.1001/archinte.168.20.2268 - DOI - PMC - PubMed
    1. Jha V, Garcia-Garcia G, Iseki K, Li Z, Naicker S, Plattner B, et al. Chronic kidney disease: global dimension and perspectives. Lancet. (2013) 382:260–72. 10.1016/S0140-6736(13)60687-X - DOI - PubMed
    1. Andrassy KM. Comments on ‘KDIGO 2012 clinical practice guideline for the evaluation and management of chronic kidney disease’. Kidney Int. (2013) 84:622–3. 10.1038/ki.2013.243 - DOI - PubMed

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