Ferritinophagy in the etiopathogenic mechanism of related diseases.

Xuemei Jin, Chunjie Jiang, Zhizhou Zou, He Huang, Xiaojian Li, Songji Xu, Rongshao Tan

Journal: The Journal of nutritional biochemistry 2023;117():109339

PMID: 37061010

Full Text on Elsevier Science View on PubMed

Abstract

Iron is an essential trace element that is involved in a variety of physiological processes. Ferritinophagy is selective autophagy mediated by nuclear receptor coactivator 4 (NCOA4), which regulates iron homeostasis in the body. Upon iron depletion or starvation, ferritinophagy is activated, releasing large amounts of Fe and increasing reactive oxygen species (ROS), leading to ferroptosis. This plays a significant role in the etiopathogenesis of many diseases, such as metabolic diseases, neurodegenerative diseases, infectious diseases, tumors, cardiomyopathy, and ischemia-reperfusion ischemia-reperfusion injury. Here, we first review the regulation and functions of ferritinophagy and then describe its involvement in different diseases, with hopes of providing new understanding and insights into iron metabolism and iron disorder-related diseases and the therapeutic opportunity for targeting ferritinophagy.

Address: Department of Preventive Medicine, School of Medicine, Yanbian University, Yanji, China; Department of Clinical Nutrition, Guangzhou Institute of Disease-Oriented Nutritional Research, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.; Department of Clinical Nutrition, Guangzhou Institute of Disease-Oriented Nutritional Research, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.; Department of Burn, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China.; Department of Preventive Medicine, School of Medicine, Yanbian University, Yanji, China.; Department of Clinical Nutrition, Guangzhou Institute of Disease-Oriented Nutritional Research, Guangzhou Red Cross Hospital of Jinan University, Guangzhou, China. Electronic address: [email protected].

DOI: 10.1016/j.jnutbio.2023.109339

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MeSH Terms: Humans, Ferritins, Nuclear Receptor Coactivators, Autophagy, Iron, Neoplasms, Transcription Factors