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血清sFRP-4水平及结缔组织生长因子与2型糖尿病肾病的关系研究进展
Progress of Research on the Relationship between Serum sFRP-4 Levels and Connective Tissue Growth Factor and Type 2 Diabetic Nephropathy

DOI: 10.12677/ACM.2023.13112464, PP. 17584-17590

Keywords: 糖尿病肾脏疾病,分泌型卷曲相关蛋白-4,结缔组织生长因子
Diabetic Kidney Disease
, Secreted Frizzled-Related Protein 4, Connective Tissue Growth Factor

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Abstract:

糖尿病肾脏疾病(diabetic kidney disease, DKD)作为糖尿病(diabetes mellitus, DM)最常见的慢性并发症之一,是引起终末期肾脏疾病(end-stage renal disease, ESRD)的主要原因。伴随DKD患者数量的增长,在很大程度上增加了ESRD的患病率。因此,早期评估DM患者的肾脏功能以便及时发现并治疗,减少DKD的患病率。本文将总结近几年关于DKD发生机制的最新进展与血清分泌型卷曲相关蛋白-4 (secreted frizzled-related protein 4, sFRP-4)及结缔组织生长因子(connective tissue growth factor, CTGF)作为检验指标与DKD的关系。
Diabetic kidney disease (DKD), as one of the most common chronic complications of diabetes melli-tus (DM), is a major cause of end-stage renal disease (ESRD). The growth in the number of patients with DKD has been accompanied by a significant increase in the prevalence of ESRD. Therefore, early assessment of renal function in DM patients allows for timely detection and treatment to re-duce the prevalence of DKD. In this paper, we will summarize the recent advances on the mecha-nism of DKD and the relationship between serum secreted frizzled-related protein 4 (sFRP-4) and connective tissue growth factor (CTGF) as tests and DKD.

References

[1]  Cho, N.H., Shaw, J.E., Karuranga, S., et al. (2018) IDF Diabetes Atlas: Global Estimates of Diabetes Prevalence for 2017 and Projections for 2045. Diabetes Research and Clinical Practice, 138, 271-281.
https://doi.org/10.1016/j.diabres.2018.02.023
[2]  中华医学会糖尿病学分会. 中国2型糖尿病防治指南(2020年版) [J]. 中华糖尿病杂志, 2021, 13(4): 315-409.
[3]  Morrish, N.J., Wang, S.L., Stevens, L.K., Fuller, J.H. and Keen, H. (2001) Mortality and Causes of Death in the WHO Multinational Study of Vascular Disease in Diabetes. Dia-betologia, 44, Article No. S14.
https://doi.org/10.1007/PL00002934
[4]  莫梓沂, 刘畅, 薛世圆, 等. 糖尿病肾病发病机制及治疗的研究进展[J]. 局解手术学杂志, 2021, 30(12): 1093-1098.
[5]  Ruiz-Ortega, M., Rodrigues-Diez, R.R., Lavoz, C. and Rayego-Mateos, S. (2020) Special Issue “Diabetic Nephropathy: Diagnosis, Prevention and Treatment”. The Journal of Clinical Medicine, 9, Article 813.
https://doi.org/10.3390/jcm9030813
[6]  Natesan, V. and Kim, S.J. (2021) Diabetic Nephropathy—A Review of Risk Factors, Progression, Mechanism, and Dietary Management. Biomolecules & Therapeutics, 29, 365-372.
https://doi.org/10.4062/biomolther.2020.204
[7]  Semba, R.D., Nicklett, E.J. and Ferrucci, L. (2010) Does Accu-mulation of Advanced Glycation End Products Contribute to the Aging Phenotype? The Journals of Gerontology: Series A, 65A, 963-975.
https://doi.org/10.1093/gerona/glq074
[8]  Uribarri, J., Cai, W., Peppa, M., et al. (2007) Circulating Glycotoxins and Dietary Advanced Glycation Endproducts: Two Links to Inflammatory Response, Oxidative Stress, and Aging. The Journals of Gerontology: Series A, 62, 427-433.
https://doi.org/10.1093/gerona/62.4.427
[9]  Ottum, M.S. and Mistry, A.M. (2015) Advanced Glycation End-Products: Modifiable Environmental Factors Profoundly Mediate Insulin Resistance. Journal of Clinical Biochemistry and Nutrition, 57, 1-12.
https://doi.org/10.3164/jcbn.15-3
[10]  Vlassara, H. and Uribarri, J. (2014) Advanced Glycation End Products (AGE) and Diabetes: Cause, Effect, or Both? Current Diabetes Reports, 14, Article No. 453.
https://doi.org/10.1007/s11892-013-0453-1
[11]  Miyata, T., Ueda, Y., Horie, K., et al. (1998) Renal Catabolism of Advanced Glycation End Products: The Fate of Pentosidine. Kidney International, 53, 416-422.
https://doi.org/10.1046/j.1523-1755.1998.00756.x
[12]  Rabbani, N. and Thornalley, P.J. (2018) Advanced Gly-cation End Products in the Pathogenesis of Chronic Kidney Disease. Kidney International, 93, 803-813.
https://doi.org/10.1016/j.kint.2017.11.034
[13]  Flyvbjerg, A. (2017) The Role of the Complement System in Dia-betic Nephropathy. Nature Reviews Nephrology, 13, 311-318.
https://doi.org/10.1038/nrneph.2017.31
[14]  Sugahara, M., Pak, W.L.W., Tanaka, T., Tang, S.C.W. and Nangaku, M. (2021) Update on Diagnosis, Pathophysiology, and Management of Diabetic Kidney Disease. Nephrology, 26, 491-500.
https://doi.org/10.1111/nep.13860
[15]  Patel, D.M., Bose, M. and Cooper, M.E. (2020) Glucose and Blood Pressure-Dependent Pathways—The Progression of Diabetic Kidney Disease. International Journal of Molecular Sciences, 21, Article 2218.
https://doi.org/10.3390/ijms21062218
[16]  Giacchetti, G., Sechi, L.A., Rilli, S. and Carey, R.M. (2005) The Ren-in-Angiotensin-Aldosterone System, Glucose Metabolism and Diabetes. Trends in Endocrinology & Metabolism, 16, 120-126.
https://doi.org/10.1016/j.tem.2005.02.003
[17]  Toma, I., Kang, J.J., Sipos, A., et al. (2008) Succinate Receptor GPR91 Provides a Direct Link between High Glucose Levels and Renin Release in Murine and Rabbit Kidney. Journal of Clinical Investigation, 118, 2526-2534.
https://doi.org/10.1172/JCI33293
[18]  Patel, D.M., Cravedi, P. and Remuzzi, G. (2010) The RAAS in the Patho-genesis and Treatment of Diabetic Nephropathy. Nature Reviews Nephrology, 6, 319-330.
https://doi.org/10.1038/nrneph.2010.58
[19]  Briet, M. and Schiffrin, E.L. (2011) The Role of Aldosterone in the Metabolic Syndrome. Current Hypertension Reports, 13, 163-172.
https://doi.org/10.1007/s11906-011-0182-2
[20]  Gurley, S.B. and Coffman, T.M. (2007) The Renin-Angiotensin System and Diabetic Nephropathy. Seminars in Nephrology, 27, 144-152.
https://doi.org/10.1016/j.semnephrol.2007.01.009
[21]  Ritz, E. and Tomaschitz, A. (2009) Aldosterone, a Vascu-lotoxic Agent—Novel Functions for an Old Hormone. Nephrology Dialysis Transplantation, 24, 2302-2305.
https://doi.org/10.1093/ndt/gfp206
[22]  Kato, M. and Natarajan, R. (2019) Epigenetics and Epigenomics in Diabetic Kidney Disease and Metabolic Memory. Nature Reviews Nephrology, 15, 327-345.
https://doi.org/10.1038/s41581-019-0135-6
[23]  Maghbooli, Z., Larijani, B., Emamgholipour, S., et al. (2014) Ab-errant DNA Methylation Patterns in Diabetic Nephropathy. Journal of Diabetes & Metabolic Disorders, 13, Article No. 69.
https://doi.org/10.1186/2251-6581-13-69
[24]  Agostino, M., Pohl, S. and Dharmarajan, A. (2017) Struc-ture-Based Prediction of Wnt Binding Affinities for Frizzled-Type Cysteine-Rich Domains. Journal of Biological Chem-istry, 292, 11218-11229.
https://doi.org/10.1074/jbc.M117.786269
[25]  Jones, S.E. and Jomary, C. (2002) Secreted Frizzled-Related Pro-teins: Searching for Relationships and Patterns. BioEssays, 24, 811-820.
https://doi.org/10.1002/bies.10136
[26]  Taneera, J., Lang, S., Sharma, A., et al. (2012) A Systems Genetics Ap-proach Identifies Genes and Pathways for Type 2 Diabetes in Human Islets. Cell Metabolism, 16, 122-134.
https://doi.org/10.1016/j.cmet.2012.06.006
[27]  Baldane, S., Ipekci, S.H., Ekin, A., et al. (2018) Evaluation of Fractalkine (FKN) and Secreted Frizzled-Related Protein 4 (SFRP-4) Serum Levels in Patients with Prediabetes and Type 2 Diabetes. Bratislava Medical Journal, 119, 112-115.
https://doi.org/10.4149/BLL_2018_021
[28]  Bukhari, S.A., Yasmin, A., Zahoor, M.A., et al. (2019) Secreted Frizzled-Related Protein 4 and Its Implication in Obesity and Type-2 Diabetes. IUBMB Life, 71, 1701-1710.
https://doi.org/10.1002/iub.2123
[29]  Mahdi, T., H?nzelmann, S., Salehi, A., et al. (2012) Secreted Frizzled-Related Protein 4 Reduces Insulin Secretion and Is Overexpressed in Type 2 Diabetes. Cell Metabolism, 16, 625-633.
https://doi.org/10.1016/j.cmet.2012.10.009
[30]  廖欢, 罗敏虹, 张伟勇, 等. 血清分泌型卷曲相关蛋白4与糖尿病肾病的关系分析[J]. 中国现代药物应用, 2019, 13(13): 43-44.
[31]  Holbourn, K.P., Acharya, K.R. and Perbal, B. (2008) The CCN Family of Proteins: Structure-Function Relationships. Trends in Bi-ochemical Sciences, 33, 461-473.
https://doi.org/10.1016/j.tibs.2008.07.006
[32]  Chen, C.C. and Lau, L.F. (2009) Functions and Mechanisms of Action of CCN Matricellular Proteins. The International Journal of Biochemistry & Cell Biology, 41, 771-783.
https://doi.org/10.1016/j.biocel.2008.07.025
[33]  Toda, N., Mukoyama, M., Yanagita, M. and Yokoi, H. (2018) CTGF in Kidney Fibrosis and Glomerulonephritis. Inflammation and Regeneration, 38, Article No. 14.
https://doi.org/10.1186/s41232-018-0070-0
[34]  Lau, L.F. and Lam, S.C. (1999) The CCN Family of Angio-genic Regulators: The Integrin Connection. Experimental Cell Research, 248, 44-57.
https://doi.org/10.1006/excr.1999.4456
[35]  Chen, P.C., Cheng, H.C., Yang, S.F., et al. (2014) The CCN Family Proteins: Modulators of Bone Development and Novel Targets in Bone-Associated Tumors. BioMed Research Interna-tional, 2014, Article ID: 437096.
https://doi.org/10.1155/2014/437096
[36]  Pan, L.H., Beppu, T., Kurose, A., et al. (2002) Neoplastic Cells and Pro-liferating Endothelial Cells Express Connective Tissue Growth Factor (CTGF) in Glioblastoma. Neurological Research, 24, 677-683.
https://doi.org/10.1179/016164102101200573
[37]  Koliopanos, A., Friess, H., di Mola, F.F., et al. (2002) Connec-tive Tissue Growth Factor Gene Expression Alters Tumor Progression in Esophageal Cancer. World Journal of Surgery, 26, 420-427.
https://doi.org/10.1007/s00268-001-0242-x
[38]  Wenger, C., Ellenrieder, V., Alber, B., et al. (1999) Expression and Differential Regulation of Connective Tissue Growth Factor in Pancreatic Cancer Cells. Oncogene, 18, 1073-1080.
https://doi.org/10.1038/sj.onc.1202395
[39]  Shakunaga, T., Ozaki, T., Ohara, N., et al. (2000) Expression of Con-nective Tissue Growth Factor in Cartilaginoustumors. Cancer, 89, 1466-1473.
https://doi.org/10.1002/1097-0142(20001001)89:7<1466::AID-CNCR8>3.0.CO;2-G
[40]  Ellina, O., Chatzigeorgiou, A., Kouyanou, S., et al. (2012) Extracellular Matrix-Associated (GAGs, CTGF), Angiogenic (VEGF) and Inflammatory Factors (MCP-1, CD40, IFN-γ) in Type 1 Diabetes Mellitus Nephropathy. Clinical Chemistry and Laboratory Medicine, 50, 167-174.
https://doi.org/10.1515/cclm.2011.881
[41]  Steffes, M.W., Osterby, R., Chavers, B., et al. (1989) Mesangial Expansion as a Central Mechanism for Loss of Kidney Function in Diabetic Patients. Diabetes, 38, 1077-1081.
[42]  Mason, R.M. and Wahab, N.A. (2003) Extracellular Matrix Metabolism in Diabetic Nephropathy. Journal of the American Society of Nephrology, 14, 1358-1373.
https://doi.org/10.1097/01.ASN.0000065640.77499.D7
[43]  Ito, Y., Aten, J., Bende, J.R., et al. (1998) Expression of Connective Tissue Growth Factor in Human Renal Fibrosis. Kidney International, 53, 853-861.
https://doi.org/10.1111/j.1523-1755.1998.00820.x
[44]  Roestenberg, P., van Nieuwenhoven, F.A., Wieten, L., et al. (2004) Connective Tissue Growth Factor Is Increased in Plasma of Type 1 Diabetic Patients with Nephropathy. Diabetes Care, 27, 1164-1170.
https://doi.org/10.2337/diacare.27.5.1164

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