Unraveling the Molecular Regulation of Ferroptosis in Respiratory Diseases

J Inflamm Res. 2024 Apr 24:17:2531-2546. doi: 10.2147/JIR.S457092. eCollection 2024.

Abstract

Ferroptosis, a type of programmed cell death that relies on iron, is distinct in terms of its morphological, biochemical and genetic features. Unlike other forms of cell death, such as autophagy, apoptosis, necrosis, and pyroptosis, ferroptosis is primarily caused by lipid peroxidation. Cells that die due to iron can potentially trigger an immune response which intensifies inflammation and causes severe inflammatory reactions that eventually lead to multiple organ failure. In recent years, ferroptosis has been identified in an increasing number of medical fields, including neurological pathologies, chronic liver diseases and sepsis. Ferroptosis has the potential to cause an inflammatory tempest, with many of the catalysts and pathological indications of respiratory ailments being linked to inflammatory reactions. The growing investigation into ferroptosis in respiratory disorders has also garnered significant interest to better understand the mechanism of ferroptosis in these diseases. In this review, the recent progress in understanding the molecular control of ferroptosis and its mechanism in different respiratory disorders is examined. In addition, this review discusses current challenges and prospects for understanding the link between respiratory diseases and ferroptosis.

Keywords: ferroptosis; iron metabolism; oxidative stress; respiratory system; treatment.

Publication types

  • Review

Grants and funding

This review was supported by ‘Jinhua Municipal Science and Technology Bureau Key Project (No. 2020-3-035, 2023-3-091) and Jinhua Municipal Central Hospital Science and Technology Project (No. JY2022-1-04).