Jin Rui, Dai Yue, Wang Zheng, Hu Qinyang, Zhang Cuntai, Gao Hongyu, Yan Qi
Department of Geriatrics, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Key Laboratory of Vascular Aging, Ministry of Education, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Biology (Basel). 2024 Dec 27;14(1):12. doi: 10.3390/biology14010012.
Chronic kidney disease (CKD) is a global health concern caused by conditions such as hypertension, diabetes, hyperlipidemia, and chronic nephritis, leading to structural and functional kidney injury. Kidney fibrosis is a common outcome of CKD progression, with abnormal fatty acid oxidation (FAO) disrupting renal energy homeostasis and leading to functional impairments. This results in maladaptive repair mechanisms and the secretion of profibrotic factors, and exacerbates renal fibrosis. Understanding the molecular mechanisms of renal fibrosis is crucial for delaying CKD progression. Ferroptosis is a type of discovered an iron-dependent lipid peroxidation-regulated cell death. Notably, Ferroptosis contributes to tissue and organ fibrosis, which is correlated with the degree of renal fibrosis. This study aims to clarify the complex mechanisms of ferroptosis in renal parenchymal cells and explore how ferroptosis intervention may help alleviate renal fibrosis, particularly by addressing the gap in CKD mechanisms related to abnormal lipid metabolism under the ferroptosis context. The goal is to provide a new theoretical basis for clinically delaying CKD progression.
慢性肾脏病(CKD)是一种全球性的健康问题,由高血压、糖尿病、高脂血症和慢性肾炎等疾病引起,导致肾脏结构和功能损伤。肾纤维化是CKD进展的常见结果,异常的脂肪酸氧化(FAO)会破坏肾脏能量稳态并导致功能障碍。这会导致适应性修复机制和促纤维化因子的分泌,并加剧肾纤维化。了解肾纤维化的分子机制对于延缓CKD进展至关重要。铁死亡是一种发现的铁依赖性脂质过氧化调节的细胞死亡。值得注意的是,铁死亡促成组织和器官纤维化,这与肾纤维化程度相关。本研究旨在阐明肾实质细胞中铁死亡的复杂机制,并探索铁死亡干预如何有助于减轻肾纤维化,特别是通过解决铁死亡背景下与异常脂质代谢相关的CKD机制方面的差距。目标是为临床上延缓CKD进展提供新的理论依据。