Regulation of pyroptosis and ferroptosis by mitophagy in chronic kidney disease.
10.11817/j.issn.1672-7347.2024.240458
- Author:
Yue HUANG
1
;
Lina YANG
2
Author Information
1. Department of Nutrition and Food Hygiene, Xiangya School of Public Health, Central South University, Changsha 410013, China. 226912055@csu.edu.cn.
2. Department of Nutrition and Food Hygiene, Xiangya School of Public Health, Central South University, Changsha 410013, China. ylnly1997@csu.edu.cn.
- Publication Type:Review
- Keywords:
cell death;
chronic kidney disease;
ferroptosis;
mitophagy;
pyroptosis
- MeSH:
Ferroptosis/physiology*;
Humans;
Renal Insufficiency, Chronic/physiopathology*;
Mitophagy/physiology*;
Pyroptosis/physiology*;
Reactive Oxygen Species/metabolism*;
Mitochondria/metabolism*;
Signal Transduction;
Animals;
Kidney/pathology*
- From:
Journal of Central South University(Medical Sciences)
2024;49(11):1769-1776
- CountryChina
- Language:English
-
Abstract:
Chronic kidney disease (CKD) is a chronic progressive disease characterized by kidney injury or declining renal function. With its insidious onset and significant harm, CKD has become a major global public health concern. Abnormal cell death can directly or indirectly contribute to kidney injury, among which excessive pyroptosis and ferroptosis are central events in CKD pathogenesis. These two forms of cell death may interact through mechanisms such as reactive oxygen species release, further aggravating renal damage. Mitophagy, a selective autophagic process that removes damaged mitochondria, plays an important role in maintaining cellular homeostasis. In CKD, mitophagy is impaired; however, enhancing mitophagy signaling pathways can alleviate inflammation, reduce iron accumulation and lipid peroxidation in renal cells. This suggests that mitophagy may be a key regulator of pyroptosis and ferroptosis in kidney cells and holds potential as a novel target for the prevention, diagnosis, and treatment of CKD.
