A Glimpse of the Mechanisms Related to Renal Fibrosis in Diabetic Nephropathy

被引：97
作者：
Zeng, Ling-Feng [1 ]
Xiao, Ying [1 ]
Sun, Lin [1 ]
机构：
[1] Cent S Univ, Xiangya Hosp 2, Dept Nephrol, Changsha, Hunan, Peoples R China
来源：
RENAL FIBROSIS: MECHANISMS AND THERAPIES | 2019年 / 1165卷
关键词：
Renal fibrosis; Diabetic nephropathy; TGF-beta; Epithelial-mesenchymal transition; miRNA; EPITHELIAL-MESENCHYMAL TRANSITION; TISSUE GROWTH-FACTOR; PROTEIN-KINASE-C; MIGRATION INHIBITORY FACTOR; JAK/STAT-SIGNALING PATHWAY; HIGH GLUCOSE; TGF-BETA; DOWN-REGULATION; MAST-CELLS; MESANGIAL CELLS;
D O I：
10.1007/978-981-13-8871-2_4
中图分类号：
R5 [内科学]; R69 [泌尿科学（泌尿生殖系疾病）];
学科分类号：
1002 ; 100201 ;
摘要：
Diabetic nephropathy (DN) is a common kidney disease in people with diabetes, which is also a serious microvascular complication of diabetes and the main cause of end-stage renal disease (ESRD) in developed and developing countries. Renal fibrosis is a finally pathological change in DN. Nevertheless, the relevant mechanism of cause to renal fibrosis in DN is still complex. In this review, we summarized that the role of cell growth factors, epithelial-mesenchymal transition (EMT) in the renal fibrosis of DN, we also highlighted the miRNA and inflammatory cells, such as macrophage, T lymphocyte, and mastocyte modulate the progression of DN. In addition, there are certain other mechanisms that may yet be conclusively defined. Recent studies demonstrated that some of the new signaling pathways or molecules, such as Notch, Wnt, mTOR, Epac-Rap-1 pathway, may play a pivotal role in the modulation of ECM accumulation and renal fibrosis in DN. This review aims to elucidate the mechanism of renal fibrosis in DN and has provided new insights into possible therapeutic interventions to inhibit renal fibrosis and delay the development of DN.
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页码：49 / 79
页数：31
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