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      The Role of Cell Division Autoantigen 1 (CDA1) in Renal Fibrosis of Diabetic Nephropathy

      review-article
      Author(s): 1 , 2 , 1 , 1 , , 2 , 3 , , 2 , 4 ,
      Publication date (Electronic):
      Journal: BioMed Research International
      Publisher: Hindawi

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          Abstract

          The common kidney disease diabetic nephropathy (DN) accounts for significant morbidity and mortality in patients with diabetes, and its effective diagnosis in incipient stages is still lacking. Renal fibrosis is the main pathological feature of DN. Cell division autoantigen 1 (CDA1), a phosphorylated protein encoded by TSPYL2 on the X chromosome, plays a fibrogenic role by modulating the transforming growth factor- β (TGF- β) signaling, but the exact mechanism remains unclear. TGF- β signaling has been recognized as the key factor in promoting the development and progression of DN. At present, strict control of blood sugar and blood pressure can significantly lower the development and progression of DN in the early stages, and many studies have shown that blocking TGF- β signaling can delay the progress of DN. However, TGF- β is a multifunctional cytokine. Its direct intervention may result in increased side effects. Therefore, the targeted intervention of CDA1 not only can block the TGF- β signaling pathway but also can reduce these side effects. In this article, we review the main physiological roles of CDA1, with particular attention to its effect and potential mechanism in the renal fibrosis of DN.

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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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            Global estimates of diabetes prevalence for 2013 and projections for 2035.

            L Guariguata, D.R. Whiting, I Hambleton … (2014)
            Diabetes is a serious and increasing global health burden and estimates of prevalence are essential for appropriate allocation of resources and monitoring of trends. We conducted a literature search of studies reporting the age-specific prevalence for diabetes and used the Analytic Hierarchy Process to systematically select studies to generate estimates for 219 countries and territories. Estimates for countries without available source data were modelled from pooled estimates of countries that were similar in regard to geography, ethnicity, and economic development. Logistic regression was applied to generate smoothed age-specific prevalence estimates for adults 20-79 years which were then applied to population estimates for 2013 and 2035. A total of 744 data sources were considered and 174 included, representing 130 countries. In 2013, 382 million people had diabetes; this number is expected to rise to 592 million by 2035. Most people with diabetes live in low- and middle-income countries and these will experience the greatest increase in cases of diabetes over the next 22 years. The new estimates of diabetes in adults confirm the large burden of diabetes, especially in developing countries. Estimates will be updated annually including the most recent, high-quality data available. Copyright © 2013. Published by Elsevier Ireland Ltd.
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              Global Prevalence of Diabetes: Estimates for the year 2000 and projections for 2030

              P S Wild, G Roglic, Carla Green … (2004)
              Article 0 comments Cited 503 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Bin Hu:
                ORCID: https://orcid.org/0000-0002-8509-6069
                Changbai Liu:
                ORCID: https://orcid.org/0000-0001-7954-0736
                Hu Wang:
                ORCID: https://orcid.org/0000-0001-6132-8788
                Journal
                Journal ID (nlm-ta): Biomed Res Int
                Journal ID (iso-abbrev): Biomed Res Int
                Journal ID (publisher-id): BMRI
                Title: BioMed Research International
                Publisher: Hindawi
                ISSN (Print): 2314-6133
                ISSN (Electronic): 2314-6141
                Publication date Collection: 2021
                Publication date (Electronic): 28 April 2021
                Volume: 2021
                Electronic Location Identifier: 6651075
                Affiliations
                1Affiliated Ren He Hospital of China Three Gorges University, Yichang 443002, China
                2Medical School, China Three Gorges University, 8 Daxue Road, Yichang 443002, China
                3Hubei Key Laboratory of Tumor Microenvironment and Immunotherapy, China Three Gorges University, 8 Daxue Road, Yichang 443002, China
                4Institute for Cell Engineering, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA
                Author notes

                Academic Editor: Kosuru Ramoji

                Author information
                https://orcid.org/0000-0002-0212-5216
                https://orcid.org/0000-0002-0053-7479
                https://orcid.org/0000-0002-8509-6069
                https://orcid.org/0000-0001-7954-0736
                https://orcid.org/0000-0001-6132-8788
                Article
                DOI: 10.1155/2021/6651075
                PMC ID: 8102118
                PubMed ID: 33997036
                SO-VID: 1b8cc82b-8ac5-465e-a7e4-c311972a8687
                Copyright © Copyright © 2021 LinLin Chen et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 17 October 2020
                Date revision received : 5 April 2021
                Date accepted : 16 April 2021
                Funding
                Funded by: Science Foundation of CTGU
                Award ID: KJ2014B066
                Funded by: National Natural Science Foundation of China
                Award ID: 81501330
                Award ID: 32071445
                Funded by: Joint Fund of Hubei Provincial Health Commission
                Award ID: WJ2019H561
                Categories
                Subject: Review Article

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