The role of innate immunity in diabetic nephropathy and their therapeutic consequences

被引:15
|
作者
Yang, Min [1 ]
Zhang, Chun [1 ]
机构
[1] Huazhong Univ Sci & Technol, Union Hosp, Tongji Med Coll, Dept Nephrol, Wuhan 430022, Peoples R China
基金
中国国家自然科学基金;
关键词
Innate immunity; Diabetic nephropathy; Inflammation; Toll -like receptor; Inflammasomes; TOLL-LIKE RECEPTORS; MANNOSE-BINDING LECTIN; NF-KAPPA-B; MONOCYTE CHEMOATTRACTANT PROTEIN-1; RENIN-ANGIOTENSIN SYSTEM; PATTERN-RECOGNITION RECEPTORS; GLOMERULAR ENDOTHELIAL-CELLS; TUBULAR EPITHELIAL-CELLS; INDUCED PODOCYTE INJURY; RENAL-FUNCTION DECLINE;
D O I
10.1016/j.jpha.2023.09.003
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Diabetic nephropathy (DN) is an enduring condition that leads to inflammation and affects a substantial number of individuals with diabetes worldwide. A gradual reduction in glomerular filtration and emergence of proteins in the urine are typical aspects of DN, ultimately resulting in renal failure. Mounting evidence suggests that immunological and inflammatory factors are crucial for the development of DN. Therefore, the activation of innate immunity by resident renal and immune cells is critical for initiating and perpetuating inflammation. Toll-like receptors (TLRs) are an important group of receptors that identify patterns and activate immune responses and inflammation. Meanwhile, inflammatory responses in the liver, pancreatic islets, and kidneys involve inflammasomes and chemokines that generate pro-inflammatory cytokines. Moreover, the activation of the complement cascade can be triggered by glycated proteins. This review highlights recent findings elucidating how the innate immune system contributes to tissue fibrosis and organ dysfunction, ultimately leading to renal failure. This review also discusses innovative approaches that can be utilized to modulate the innate immune responses in DN for therapeutic purposes. (c) 2023 The Author(s). Published by Elsevier B.V. on behalf of Xi'an Jiaotong University. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
引用
收藏
页码:39 / 51
页数:13
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