Biochemistry of mammalian ferritins in the regulation of cellular iron homeostasis and oxidative responses

Jianlin Zhang, Xuehui Chen, Juanji Hong, Aifa Tang, Yang Liu, Ni Xie*, Guohui Nie*, Xiyun Yan*, Minmin Liang*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

54 Citations (Scopus)

Abstract

Ferritin, an iron-storage protein, regulates cellular iron metabolism and oxidative stress. The ferritin structure is characterized as a spherical cage, inside which large amounts of iron are deposited in a safe, compact and bioavailable form. All ferritins readily catalyze Fe(II) oxidation by peroxides at the ferroxidase center to prevent free Fe(II) from participating in oxygen free radical formation via Fenton chemistry. Thus, ferritin is generally recognized as a cytoprotective stratagem against intracellular oxidative damage The expression of cytosolic ferritins is usually regulated by iron status and oxidative stress at both the transcriptional and post-transcriptional levels. The mechanism of ferritin-mediated iron recycling is far from clarified, though nuclear receptor co-activator 4 (NCOA4) was recently identified as a cargo receptor for ferritin-based lysosomal degradation. Cytosolic ferritins are heteropolymers assembled by H- and L-chains in different proportions. The mitochondrial ferritins are homopolymers and distributed in restricted tissues. They play protective roles in mitochondria where heme- and Fe/S-enzymes are synthesized and high levels of ROS are produced. Genetic ferritin disorders are mainly related to the L-chain mutations, which generally cause severe movement diseases. This review is focused on the biochemistry and function of mammalian intracellular ferritin as the major iron-storage and anti-oxidation protein.

Original languageEnglish
Pages (from-to)352-362
Number of pages11
JournalScience China Life Sciences
Volume64
Issue number3
DOIs
Publication statusPublished - Mar 2021

Keywords

  • Fenton reaction
  • antioxidant
  • ferritin
  • iron homeostasis
  • oxidative responses

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