Research progress of ferroptosis and inflammatory bowel disease

被引:1
|
作者
Ma, Baolian [1 ]
Hu, Xiaoxue [1 ]
Ai, Xiaowen [1 ]
Zhang, Yonglan [1 ]
机构
[1] Chongqing Univ Technol, Coll Pharm & Bioengn, Chongqing, Peoples R China
基金
中国国家自然科学基金;
关键词
Inflammatory bowel disease; Ferroptosis; Lipid peroxide; Therapeutic target; INDUCED ULCERATIVE-COLITIS; GENOME-WIDE ASSOCIATION; CANCER-CELL DEATH; OXIDATIVE STRESS; IRON; RISK; GENETICS; CROHNS; SENSITIVITY; INHIBITION;
D O I
10.1007/s10534-024-00604-2
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Inflammatory bowel disease (IBD) is a non-specific chronic inflammatory disorder of the gastrointestinal tract, imposing significant burdens on both society and individuals. As a new type of regulated cell death (RCD), ferroptosis is different from classic RCDs such as apoptosis and necrosis in cell morphology, biochemistry and genetics. The main molecular mechanisms of ferroptosis include dysregulation of iron metabolism, impaired antioxidant capacity, mitochondrial dysfunction, accumulation of lipid-associated super-oxides, and membrane disruption. In recent years, increasing evidence has shown that ferroptosis is involved in the pathophysiology of inflammatory bowel disease. However, the exact roles and underlying molecular mechanisms have not been fully elucidated. This article reviews the mechanism of ferroptosis in the occurrence and development of inflammatory bowel disease, in order to provide new ideas for the pathophysiological research of inflammatory bowel disease. Additionally, we discuss potential strategies for the prevention and treatment of inflammatory bowel disease by targeting ferroptosis.
引用
收藏
页码:1039 / 1062
页数:24
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