Nrf2 attenuates ferroptosis-mediated IIR-ALI by modulating TERT and SLC7A11
Open accessAbstract
Acute lung injury (ALI) carries a mortality rate of ~50% and is a hot topic in the world of critical illness research. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a critical modulator of intracellular oxidative homeostasis and serves as an antioxidant. The Nrf2-related anti-oxidative stress is strongly associated with ferroptosis suppression. Meanwhile, telomerase reverse transcriptase (TERT), the catalytic portion of the telomerase protein, is reported to travel to the mitochondria to alleviate ROS. In our study, we found that TERT was significantly reduced in lung tissue of Nrf2 −/− mice in the model of intestinal ischemia/reperfusion-induced acute lung injury (IIR-ALI). In addition, MDA levels showed marked increase, whereas GSH and GPX4 levels fell drastically in ALI models. Moreover, typical-related structural changes were observed in the type II alveolar epithelial cells in the IIR model. We further employed the scanning transmission X-ray microscopy (STXM) to examine Fe levels and distribution within cells. Based on our observations, massive aggregates of Fe were found in the MLE-12 cells upon OGD/R (oxygen and glucose deprivation/reperfusion) induction. Additionally, Nrf2 silencing dramatically reduced TERT and SLC7A11 levels, and further exacerbated cellular injuries. In contrast, TERT-overexpressing cells exhibited marked elevation in SLC7A11 levels and thereby inhibited ferroptosis. Collectively, these data suggest that Nrf2 can negatively regulate ferroptosis via modulation of TERT and SLC7A11 levels. The conclusion from this study brings insight into new candidates that can be targeted in future IIR-ALI therapy.
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All ApoE isoforms increased the expression of known NRF2 target genes including SLC7A11, AKR1C1, and FTH1.
“and increased the expression of known target genes of this transcription factor including SLC7A11, AKR1C1, and FTH1 (fig. S5S) (41–45).”
From Secreted Apoe rewires melanoma cell state vulnerability to ferroptosis (2024) · cites this paper as [44]
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Self-citation
- Authors
- Dong, H., Xia, Y., Jin, S., Xue, C., Wang, Y., Hu, R., & Jiang, H.
- Affiliations
- Shanghai Jiao Tong University (CN)
- Chinese Academy of Sciences (CN)
- Corresponding author
- Hu, Rong
- Jiang, Hong
- Venue
- Cell Death & Disease
- Published
- 2021-10-29
- Volume
- 12
- Issue
- 11
- Pages
- 1027-1027
- ISSN
- 2041-4889 (ISSN-L)
- PMC
- PMC8556385
- OpenAlex
- W3209906264
- Cited by
- 196
- References
- 35
- Citations by year
- 2026: 29 · 2025: 40 · 2024: 65 · 2023: 36 · 2022: 26
- FWCI
- 21.10
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Cell Death and Disease (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Science and Technology Commission of Shanghai Municipality (19ZR1476500)
- National Natural Science Foundation of China (81970065)
- Youth Innovation Promotion Association of the Chinese Academy of Sciences (2017306)
- the Incentive Project of High-level Innovation Team for Shanghai Jiao Tong University School of Medicine
- Topics
- Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Ferroptosis and cancer prognosis
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics, phytochemicals, and oxidative stress
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Keywords
- Nrf2, ferroptosis, telomerase reverse transcriptase, SLC7A11, telomerase, oxidative stress, iron accumulation, GPX4, glutathione, alveolar epithelial cells, Nrf2 knockout mice
- MeSH terms
- Ferroptosis, Animals, Cell Line, Transformed, Disease Models, Animal, Glucose, Intestines, Iron, Mice, Inbred C57BL, Oxygen, Signal Transduction, Reperfusion Injury, Mice, Knockout, Telomerase, Gene Silencing, Amino Acid Transport System y+, NF-E2-Related Factor 2, Mice, Acute Lung Injury, Alveolar Epithelial Cells
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