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The Complement System in Metabolic-Associated Kidney Diseases

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Journal Front Immunol
Date 2022 Aug 4
PMID 35924242
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Abstract

Metabolic syndrome (MS) is a group of clinical abnormalities characterized by central or abdominal obesity, hypertension, hyperuricemia, and metabolic disorders of glucose or lipid. Currently, the prevalence of MS is estimated about 25% in general population and is progressively increasing, which has become a challenging public health burden. Long-term metabolic disorders can activate the immune system and trigger a low-grade chronic inflammation named "metaflammation." As an important organ involved in metabolism, the kidney is inevitably attacked by immunity disequilibrium and "metaflammation." Recently, accumulating studies have suggested that the complement system, the most important and fundamental component of innate immune responses, is actively involved in the development of metabolic kidney diseases. In this review, we updated and summarized the different pathways through which the complement system is activated in a series of metabolic disturbances and the mechanisms on how complement mediate immune cell activation and infiltration, renal parenchymal cell damage, and the deterioration of renal function provide potential new biomarkers and therapeutic options for metabolic kidney diseases.

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References
1.
Jordan S, Choi J, Aubert O, Haas M, Loupy A, Huang E . A phase I/II, double-blind, placebo-controlled study assessing safety and efficacy of C1 esterase inhibitor for prevention of delayed graft function in deceased donor kidney transplant recipients. Am J Transplant. 2018; 18(12):2955-2964. DOI: 10.1111/ajt.14767. View

2.
Sacks S, Zhou W, Pani A, Campbell R, Martin J . Complement C3 gene expression and regulation in human glomerular epithelial cells. Immunology. 1993; 79(3):348-54. PMC: 1421987. View

3.
Biglarnia A, Huber-Lang M, Mohlin C, Ekdahl K, Nilsson B . The multifaceted role of complement in kidney transplantation. Nat Rev Nephrol. 2018; 14(12):767-781. DOI: 10.1038/s41581-018-0071-x. View

4.
Klanke B, Cordasic N, Hartner A, Schmieder R, Veelken R, Hilgers K . Blood pressure versus direct mineralocorticoid effects on kidney inflammation and fibrosis in DOCA-salt hypertension. Nephrol Dial Transplant. 2008; 23(11):3456-63. DOI: 10.1093/ndt/gfn301. View

5.
Yu S, Wang D, Huang L, Zhang Y, Luo R, Adah D . The complement receptor C5aR2 promotes protein kinase R expression and contributes to NLRP3 inflammasome activation and HMGB1 release from macrophages. J Biol Chem. 2019; 294(21):8384-8394. PMC: 6544858. DOI: 10.1074/jbc.RA118.006508. View