Roles of ferroptosis in the development of diabetic nephropathy.
10.3724/zdxbyxb-2024-0114
- Author:
Pan LIU
1
;
Zhengdong ZHANG
2
;
Qiu CHEN
3
Author Information
1. Department of Endocrinology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610072, China. liupan@stu.cdutcm.edu.cn.
2. Department of Orthopedics, School of Clinical Medicine, The First Affiliated Hospital of Chengdu Medical College, Chengdu 610500, China. zhangzd@cmc.edu.cn.
3. Department of Endocrinology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu 610072, China. chenqiu1005@cdutcm.edu.cn.
- Publication Type:English Abstract
- Keywords:
Cell death;
Diabetic nephropathy;
Ferroptosis;
Review;
Signaling pathway
- MeSH:
Diabetic Nephropathies/etiology*;
Ferroptosis;
Humans;
Signal Transduction;
Heme Oxygenase-1/genetics*;
NF-E2-Related Factor 2/metabolism*;
AMP-Activated Protein Kinases/metabolism*;
Transforming Growth Factor beta1/metabolism*;
MicroRNAs/metabolism*;
RNA, Long Noncoding/genetics*;
Hypoxia-Inducible Factor 1, alpha Subunit/metabolism*;
Lipid Peroxidation;
Animals
- From:
Journal of Zhejiang University. Medical sciences
2024;53(6):708-714
- CountryChina
- Language:Chinese
-
Abstract:
Diabetic nephropathy is a common microvascular complication of diabetes mellitus and one of the main causes of death in patients with diabetes mellitus. Ferroptosis is a newly discovered iron-dependent regulated cell death, which may contribute to the pathogenesis and development of diabetic nephropathy. Adenosine monophosphate-activated protein kinase (AMPK)-mediated ferroptosis-related signaling pathways can slow down the progression of diabetic nephropathy, but excessive activation of AMPK signaling pathway may induce cells to undergo autophagic death. Activation of the signaling pathway mediated by nuclear factor-erythroid 2-related factor (Nrf) 2 and heme oxygenase (HO)-1 can inhibit ferroptosis of cells and alleviate diabetic nephropathy. However, the regulatory effect of HO-1 on ferroptosis is bidirectional, and activation of HIF-1α/HO-1 pathway may lead to intracellular iron overload and ultimately promote ferroptosis. Transforming growth factor (TGF)-β1 mediated signaling pathways can accelerate lipid peroxidation by down-regulating the levels of SLC7A11/GSH/GPX4. The ferroptosis-related signaling pathways mediated by exosome lncRNAs/circRNAs/miRNAs are also involved in the pathogenesis and development of diabetic nephropathy. In addition, signaling pathways mediated by stimulator of interferon gene (STING) and the novel ferroptosis promoter acyl-CoA synthetase long-chain family (ACSL) 1 can induce ferroptosis to promote the progression of diabetic nephropathy. In this review, we focus on the roles of ferroptosis in diabetic nephropathy through the signaling pathways mediated by AMPK, Nrf2/HO-1, TGF-β and exosomes, to elaborate the pathogenesis and development of diabetic nephropathy, and the potential therapeutic target for diabetic nephropathy.
