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      Epigenetics in the pathogenesis of diabetic nephropathy : Epigenetics in the pathogenesis of diabetic nephropathy

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          Abstract

          Diabetic nephropathy (DN), which is a common microvascular complication with a high incidence in diabetic patients, greatly increases the mortality of patients. With further study on DN, it is found that epigenetics plays a crucial role in the pathophysiological process of DN. Epigenetics has an important impact on the development of DN through a variety of mechanisms, and promotes the generation and maintenance of metabolic memory, thus ultimately leading to a poor prognosis. In this review we discuss the methylation of DNA, modification of histone, and regulation of non-coding RNA involved in the progress of cell dysfunction, inflammation and fibrosis in the kidney, which ultimately lead to the deterioration of DN.

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          Unique features of long non-coding RNA biogenesis and function.

          Jeffrey Quinn, Howard Y. Chang (2016)
          Long non-coding RNAs (lncRNAs) are a diverse class of RNAs that engage in numerous biological processes across every branch of life. Although initially discovered as mRNA-like transcripts that do not encode proteins, recent studies have revealed features of lncRNAs that further distinguish them from mRNAs. In this Review, we describe special events in the lifetimes of lncRNAs - before, during and after transcription - and discuss how these events ultimately shape the unique characteristics and functional roles of lncRNAs.
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            RNA maps reveal new RNA classes and a possible function for pervasive transcription.

            Philipp Kapranov, Jill Cheng, Sujit Dike … (2007)
            Significant fractions of eukaryotic genomes give rise to RNA, much of which is unannotated and has reduced protein-coding potential. The genomic origins and the associations of human nuclear and cytosolic polyadenylated RNAs longer than 200 nucleotides (nt) and whole-cell RNAs less than 200 nt were investigated in this genome-wide study. Subcellular addresses for nucleotides present in detected RNAs were assigned, and their potential processing into short RNAs was investigated. Taken together, these observations suggest a novel role for some unannotated RNAs as primary transcripts for the production of short RNAs. Three potentially functional classes of RNAs have been identified, two of which are syntenically conserved and correlate with the expression state of protein-coding genes. These data support a highly interleaved organization of the human transcriptome.
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              TGF-β: the master regulator of fibrosis.

              Xiao-ming Meng, David J Nikolic-Paterson, Hui-Yao Lan (2016)
              Transforming growth factor-β (TGF-β) is the primary factor that drives fibrosis in most, if not all, forms of chronic kidney disease (CKD). Inhibition of the TGF-β isoform, TGF-β1, or its downstream signalling pathways substantially limits renal fibrosis in a wide range of disease models whereas overexpression of TGF-β1 induces renal fibrosis. TGF-β1 can induce renal fibrosis via activation of both canonical (Smad-based) and non-canonical (non-Smad-based) signalling pathways, which result in activation of myofibroblasts, excessive production of extracellular matrix (ECM) and inhibition of ECM degradation. The role of Smad proteins in the regulation of fibrosis is complex, with competing profibrotic and antifibrotic actions (including in the regulation of mesenchymal transitioning), and with complex interplay between TGF-β/Smads and other signalling pathways. Studies over the past 5 years have identified additional mechanisms that regulate the action of TGF-β1/Smad signalling in fibrosis, including short and long noncoding RNA molecules and epigenetic modifications of DNA and histone proteins. Although direct targeting of TGF-β1 is unlikely to yield a viable antifibrotic therapy due to the involvement of TGF-β1 in other processes, greater understanding of the various pathways by which TGF-β1 controls fibrosis has identified alternative targets for the development of novel therapeutics to halt this most damaging process in CKD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Acta Biochim Biophys Sin (Shanghai)
                Journal ID (iso-abbrev): Acta Biochim Biophys Sin (Shanghai)
                Journal ID (publisher-id): ABBS
                Title: Acta Biochimica et Biophysica Sinica
                Publisher: Oxford University Press
                ISSN (Print): 1672-9145
                ISSN (Electronic): 1745-7270
                Publication date (Electronic): 23 December 2021
                Publication date Collection: February 2022
                Publication date PMC-release: 23 December 2021
                Volume: 54
                Issue: 2
                Pages: 163-172
                Affiliations
                [ ] orgname1.Department of Anesthesiology orgnameFudan University Shanghai Cancer Center; Department of Oncology orgnameShanghai Medical College orgnameFudan University Shanghai 200032 China
                [ ] orgname2.Department of Anesthesiology orgnameShanghai General Hospital orgnameShanghai Jiao Tong University School of Medicine Shanghai 200080 China
                [ ] orgname3.Department of Anesthesiology orgnameEye & ENT Hospital orgnameFudan University Shanghai 200031 China
                Author notes
                Correspondence address. Tel: +86-21-6417-5590; E-mail: (M.Z.) / E-mail: (Y.Z.)zhu_mm@126.comzhao_yanjun@163.com
                Article
                DOI: 10.3724/abbs.2021016
                PMC ID: 9909329
                PubMed ID: 35130617
                SO-VID: 06527545-0b8a-4bd8-8648-71faf30487da
                Copyright © © The Author(s) 2021.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution License ( https://creativecommons.org/licenses/by/4.0/).

                History
                Date received : 8 June 2021
                Date accepted : 20 July 2021
                Funding
                Funded by: the grants from the National Science Foundation of China
                Award ID: No.
                Award ID: 81871590
                Funded by: Shanghai Sailing Program
                Award ID: No.
                Award ID: 20YF1407800
                This work was supported by the grants from the National Science Foundation of China (No. 81871590) and Shanghai Sailing Program (No. 20YF1407800).
                Categories
                Subject: Research Article
                Custom metadata
                Citation X Li, L Lu, W Hou, T Huang, X Chen, J Qi, Y Zhao, et al.Epigenetics in the pathogenesis of diabetic nephropathy. Acta Biochim Biophys Sin , 2022, 54, 163-172, https://doi.org/10.3724/abbs.2021016
                Crossmark 2021/11/8 13:44:31
                AuthorMark Li
                AuthorMarkCite X Li, L Lu, W Hou, T Huang, X Chen, J Qi, Y Zhao, et al.
                article-title Epigenetics in the pathogenesis of diabetic nephropathy

                Keywords: diabetes,diabetic nephropathy,epigenetics,metabolic memory
                Data availability:
                Keywords: diabetes, diabetic nephropathy, epigenetics, metabolic memory

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