补体因子H相关蛋白1在足细胞疾病中的研究进展
Research Progress of Complement Factor H-Related Protein 1 in Podocyte Diseases
摘要: 足细胞疾病(podocytopathies)是指直接或间接的足细胞损伤导致蛋白尿的肾脏疾病。国内外许多学者发现补体系统与足细胞损伤相关,补体因子H (complement factor H, CFH)及补体因子H相关蛋白1 (complement factor H-related 1, CFHR1)是补体替代途径激活过程中起重要调节作用的血浆蛋白。CFHR1在足细胞疾病中的发病机制至今仍不清楚,目前研究发现补体替代途径所介导的炎症反应可能起到关键作用,而CFHR1是补体替代途径激活过程中重要的调节物质。本文对CFHR1在足细胞疾病中的作用进行综述,以期为相关足细胞疾疾病的诊断和治疗提供参考。
Abstract: Podocytopathies refer to kidney diseases that lead to proteinuria due to direct or indirect podocyte injury. Many scholars at home and abroad have found that the complement system is related to podocyte injury, and complement factor H (CFH) and complement factor H-related protein 1 (CFHR1) are plasma proteins that play an important regulatory role in the activation of the complement alternative pathway. The pathogenesis of CFHR1 in podocytopathies is still unclear. Current research has found that the inflammatory response mediated by the complement alternative pathway may play a key role, and CFHR1 is an important regulatory substance in the activation process of the complement alternative pathway. This article summarizes the role of CFHR1 in podocytopathies, aiming to provide reference value for the diagnosis and treatment of related podocyte diseases.
文章引用:欧云塔娜, 张蕾, 迪丽努尔·图尔荪托合提, 周洪, 张莉. 补体因子H相关蛋白1在足细胞疾病中的研究进展[J]. 临床医学进展, 2024, 14(3): 1956-1960. https://doi.org/10.12677/acm.2024.143929

参考文献

[1] Kopp, J.B., Anders, H.-J., Susztak, K., Podestà, M.A., Remuzzi, G., Hildebrandt, F. and Romagnani, P. (2020) Podocytopathies. Nature Reviews Disease Primers, 6, Article No. 68. [Google Scholar] [CrossRef] [PubMed]
[2] 安梦丽, 何平. 足细胞损伤的机制及与肾小球疾病的关系研究进展[J]. 中国临床研究, 2018, 31(10): 1427-1431.
[3] 李卫国, 李宇宁. 足细胞对损伤的反应[J]. 临床儿科杂志, 2012, 30(11): 1091-1094.
[4] Mundel, P. and Shankland, S.J. (2002) Podocyte Biology and Response to Injury. Journal of the American Society of Nephrology, 13, 3005-3015. [Google Scholar] [CrossRef
[5] Vignesh, P., Rawat, A., Sharma, M., et al. (2017) Complement in Autoimmune Diseases. Clinica Chimica Acta, 465, 123-130. [Google Scholar] [CrossRef] [PubMed]
[6] Józsi, M., Schneider, A.E., et al. (2019) Complement Factor H Family Proteins in Their Non-Canonical Role as Modulators of Cellular Functions. Seminars in Cell & Developmental Biology, 85, 122-131. [Google Scholar] [CrossRef] [PubMed]
[7] Ferreiraa, V.P., Pangburnb, M.K. and Cortésa, C. (2010) Complement Control Protein Factor H: The Good, the Bad, and the Inadequat. Molecular Immunology, 47, 2187-2197. [Google Scholar] [CrossRef] [PubMed]
[8] Skerka, C., Chen, Q., Fremeaux-Bacchi, V., et al. (2013) Complement Factor H Related Proteins (CFHRS). Molecular Immunology, 56, 170-180. [Google Scholar] [CrossRef] [PubMed]
[9] Hannan, J.P., Laskowski, J., Thurman, J.M., et al. (2016) Mapping the Complement Factor H-Related Protein 1 (CFHR1):C3b/C3d Interactions. PLOS ONE, 11, e0166200. [Google Scholar] [CrossRef] [PubMed]
[10] Kerjaschki, D., Schulze, M. and Binder, S. (1989) Transcellular Transport and Membrane Insertion of the C5b-9 Membrane Attack Complex of Complement by Glomerular Epithelial Cells in Experimental Membranous Nephropathy. The Journal of Immunology, 143, 546-552. [Google Scholar] [CrossRef
[11] Leenaerts, P.L., Hall, B.M. and Van Damme, B.J. (1995) Active Heymann Nephritis in Complement Component C6 Deficient Rats. Kidney International, 47, 1604-1614. [Google Scholar] [CrossRef] [PubMed]
[12] Ronco, P. and Debiec, H. (2017) A Podocyte View of Membranous Nephropathy: From Heymann Nephritis to the Childhood Human Disease. Pflügers Archiv, 469, 997-1005. [Google Scholar] [CrossRef] [PubMed]
[13] Hofer, J., Janecke, A.R., Zimmerhackl, L.B., et al. (2013) Complement Factor H-Related Protein 1 Deficiency and Factor H Antibodies in Pediatric Patients with Atypical Hemolytic Uremic Syndrome. Clinical Journal of the American Society of Nephrology, 8, 407-415. [Google Scholar] [CrossRef
[14] Dragon-Durey, M.A., Blanc, C., Marliot, F., et al. (2009) The High Frequency of Complement Factor H Related CFHR1 Gene Deletion Is Restricted to Specific Subgroups of Patients with Atypical Haemolytic Uraemic Syndrome. Journal of Medical Genetics, 46, 447-450. [Google Scholar] [CrossRef] [PubMed]
[15] Eyler, S.J., Meyer, N.C., Zhang, Y., et al. (2013) A Novel Hybrid CFHR1/CFH Gene Causes Atypical Hemolytic Uremic Syndrome. Pediatric Nephrology, 28, 2221-2225. [Google Scholar] [CrossRef] [PubMed]
[16] 朱旭, 李丹丹, 邱玲. 补体因子H相关蛋白1的研究进展[J]. 临床检验杂志, 2020, 38(4): 280-282.
[17] Beck, L.H., Bonegio, R.G., Lambeau, G., Beck, D.M., Powell, D.W., Cummins, T.D., et al. (2009) M-Type Phospholipase A2 Receptor as Target Antigen in Idiopathic Membranous Nephropathy. The New England Journal of Medicine, 361, 11-21. [Google Scholar] [CrossRef
[18] Fresquet, M., Jowitt, T.A., Gummadova, J., Collins, R., O’Cualain, R., McKenzie, E.A., et al. (2015) Identification of a Major Epitope Recognized by PLA2R Autoantibodies in Primary Membranous Nephropathy. Journal of the American Society of Nephrology, 26, 302-313. [Google Scholar] [CrossRef
[19] Zhu, P., Zhou, F.D., Wang, S.X., et al. (2015) Increasing Frequency of Idiopathic Membranous Nephropathy in Primary Glomerular Disease: A 10-Year Renal Biopsy Study from a Single Chinese Nephrology Centre. Nephrology (Carlton), 20, 560-566. [Google Scholar] [CrossRef] [PubMed]
[20] Thurman, J.M. and Nester, C.M. (2016) All Things Complement. Clinical Journal of the American Society of Nephrology, 11, 1856-1866. [Google Scholar] [CrossRef
[21] Keir, L.S., Firth, R., Aponik, L., Feitelberg, D., Sakimoto, S., Aguilar, E., et al. (2017) VEGF Regulates Local Inhibitory Complement Proteins in the Eye and Kidney. Journal of Clinical Investigation, 127, 199-214. [Google Scholar] [CrossRef
[22] Cserhalmi, M., Papp, A., Brandus, B., et al. (2019) Regulation of Regulators: Role of the Complement Factor H-Related Proteins. Seminars in Immunology, 45, Article ID: 101341. [Google Scholar] [CrossRef] [PubMed]
[23] Zhu, L., Zhai, Y.L., Wang, F.M., et al. (2015) Variants in Complement Factor H and Complement Factor H-Related Protein Genes, CFHR3 and CFHR1, Affect Complement Activation in IgA Nephropathy. American Society of Nephrology, 26, 1195-1204. [Google Scholar] [CrossRef
[24] Xie, J., Kiryluk, K., Li, Y., et al. (2016) Fine Mapping Implicates a Deletion of CFHR1 and CFHR3 in Protection from IgA Nephropathy in Han Chinese. American Society of Nephrology, 27, 3187-3194. [Google Scholar] [CrossRef
[25] Jennifer, C., Haas, M., Reich, H.N., et al. (2017) Ig A Nephropathy. Clinical Journal of the American Society of Nephrology, 12, 677-686. [Google Scholar] [CrossRef
[26] 郑笑, 张艳君, 杨淑芬, 等. 补体因子H和补体因子H相关蛋白1、2、3和5与IgA肾病的关联性[J]. 实用医学杂志, 2018, 34(22): 3727-3730.
[27] Gharavi, A.G., Kiryluk, K., Choi, M., et al. (2011) Genome-Wide Association Study Identifies Susceptibility Loci for IgA Nephropathy. Nature Genetics, 43, 321-327. [Google Scholar] [CrossRef] [PubMed]