Page 308 - EJMO-9-3

Eurasian Journal of Medicine

and Oncology

LETTER TO EDITOR
Ferroptosis inhibition: New insights for the

treatment of acute lung injury

Xuhan Chen and Jinhe Guo*
Department in Traditional Chinese Medicine, College of Traditional Chinese Medicine, Tianjin
University of Traditional Chinese Medicine, Tianjin, China

Dear Editor,
In recent years, the incidence of acute lung injury (ALI) during clinical treatment has
shown a notable upward trend. The aging of the global population, the widespread use of
mechanical ventilation, and the emergence of novel pathogens have further exacerbated
this situation, posing a severe threat to public health. Consequently, identifying new
drug targets and treatment strategies for ALI has become an urgent challenge in the
medical field.
Ferroptosis, a distinct form of programmed cell death characterized by iron dependence
and lipid peroxidation, differs fundamentally from apoptosis, necrosis, and autophagy,
representing a unique mechanism of cell demise. Research indicates that ferroptosis
1
is involved in the occurrence and progression of ALI induced by various factors, such
as radiation-induced ALI, ischemia-reperfusion ALI, and lipopolysaccharide (LPS)-
2,3
induced ALI. In a sepsis-induced ALI rat model, abnormal expression of ferroptosis-
associated proteins was detected in lung tissues. Notably, pharmacological or genetic
inhibition of ferroptosis led to a marked alleviation of ALI symptoms, suggesting that
targeted modulation of ferroptosis could be a promising therapeutic approach for ALI. 4,5
*Corresponding author:
Jinhe Guo Nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) play
(guojinhe@tjutcm.edu.cn) pivotal roles as antioxidant regulators, modulating intracellular iron concentration and
4
Citation: Chen X, Guo J. metabolism, protecting cells from oxidative stress damage, and inhibiting ferroptosis. The
Ferroptosis inhibition: New insights downstream factor solute carrier family 7 member 11 (SLC7A11), a downstream effector
for the treatment of acute lung
injury. Eurasian J Med Oncol. of this regulatory network, is recognized for its inhibitory function in ferroptosis. As a
2025;9(3):300-301. key subunit of the cystine/glutamate antiporter system (system xc⁻), SLC7A11 facilitates
doi: 10.36922/EJMO025090043 the uptake of extracellular cystine into cells. In addition, glutathione peroxidase 4
Received: February 28, 2025 (GPX4) is a key protein that inhibits ferroptosis. Regulating certain pathways or directly
Accepted: March 10, 2025 targeting the activation of Nrf2 can inhibit ferroptosis and reduce lung injury. For
example, obacunone can target and activate Nrf2, inhibit the ubiquitination hydrolysis
Published Online: April 4, 2025 of Nrf2, and improve the antioxidant capacity of lung tissue. Similarly, pachymic acid,
Copyright: © 2025 Author(s). glycyrrhizic acid, curcumin, and marmesin regulate different signaling pathways to
This is an Open-Access article upregulate the expression of Nrf2, HO-1, GPX4, and SLC7A11 or downregulate the
distributed under the terms of the
Creative Commons Attribution expression of kelch-like ECH-associated protein 1 to reduce ferroptosis levels.
License, permitting distribution,
and reproduction in any medium, While the concept of ferroptosis is not explicitly defined within the theoretical
provided the original work is framework of traditional Chinese medicine (TCM), the application of TCM decoctions
properly cited. has demonstrated beneficial effects of inhibiting ferroptosis in the treatment of ALI. For
Publisher’s Note: AccScience instance, Huanglian-Jie-du Tang (HLJDD) has been utilized in the management of sepsis-
Publishing remains neutral with induced ALI, Ganlu Qingwen Fang in LPS-induced ALI, and modified Taoren Chengqi
regard to jurisdictional claims in
published maps and institutional in ventilator-induced lung injury (VILI). Modern pharmacological investigations have
affiliations. revealed that quercetin, a primary monomeric component of HLJDD, exhibits notable

Volume 9 Issue 3 (2025) 300 doi: 10.36922/EJMO025090043