The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Role of TLR4/NADPH oxidase 4 pathway in promoting cell death through autophagy and ferroptosis during heart failure
Abstract
Loss of myocytes caused by cell death plays a key role during heart failure (HF). Activated autophagy and increased ferroptosis have been observed in HF and proved to promote its progression. However, the underlying mechanisms remain unclear. Here, results from integrated bioinformatical analysis showed TLR4 and NADPH oxidase 4 (NOX4) were included in up-regulated differentially expressed genes (DEGs), and had an interaction between each other inferred by the DEGs-associated protein-protein interaction (PPI) network. To explore the role of TLR4-NOX4 in autophagy and ferroptosis, knock-down of TLR4 and NOX4 through lentiviral delivery of siRNA to the myocardium were applied respectively in HF rats induced by aortic banding, and the indicators of autophagy and ferroptosis were detected. Results revealed that either TLR4 or NOX4 knock-down significantly improved left ventricular remodeling and reduced myocytes death. Simultaneously, activated autophagy and ferroptosis in rats with HF were remarkably retarded by either TLR4 and NOX4 knock-down, suggesting TLR4-NOX4 as a potential therapeutic target for HF through inhibiting autophagy- and ferroptosis-mediated cell death.
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Ferroptosis: An Iron-Dependent Form of Nonapoptotic Cell Death
Dixon, S. J., Lemberg, K. M., Lamprecht, M. R., Skouta, R., Zaitsev, E. M., Gleason, C. E., Patel, D. N., Bauer, A. J., Cantley, A. M., Yang, W. S., et al. (2012) · Cell · doi:10.1016/j.cell.2012.03.042 · Cited by 18,691
Regulation of Ferroptotic Cancer Cell Death by GPX4
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Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease
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Ferroptosis: process and function
Xie, Y., Hou, W., Song, X., Yu, Y., Huang, J., Sun, X., Kang, R., & Tang, D. (2016) · Cell Death & Differentiation · doi:10.1038/cdd.2015.158 · Cited by 3,727
Autophagy and the Integrated Stress Response
Kroemer, G., Mariño, G., & Levine, B. (2010) · Molecular Cell · doi:10.1016/j.molcel.2010.09.023 · Cited by 3,506
NOX enzymes and the biology of reactive oxygen
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Autophagy promotes ferroptosis by degradation of ferritin
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Ferroptosis, a new form of cell death: opportunities and challenges in cancer
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Ferroptosis is an autophagic cell death process
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Cited by
The molecular and metabolic landscape of iron and ferroptosis in cardiovascular disease
Fang, X., Ardehali, H., Min, J., & Wang, F. (2023) · Nature Reviews Cardiology · doi:10.1038/s41569-022-00735-4 · Cited by 1,081
Signaling pathways and defense mechanisms of ferroptosis
Liu, J., Kang, R., & Tang, D. (2022) · The FEBS Journal · doi:10.1111/febs.16059 · Cited by 787
The emerging role of ferroptosis in inflammation
Sun, Y., Chen, P., Zhai, B., Zhang, M., Xiang, Y., Fang, J., Xu, S., Gao, Y., Chen, X., Sui, X., et al. (2020) · Biomedicine & Pharmacotherapy · doi:10.1016/j.biopha.2020.110108 · Cited by 739
Self-citationIron Homeostasis and Ferroptosis in Human Diseases: Mechanisms and Therapeutic Prospects
Ru, Q., Li, Y., Chen, L., Wu, Y., Min, J., & Wang, F. (2024) · Signal Transduction and Targeted Therapy · doi:10.1038/s41392-024-01969-z · Cited by 724
Oxidative Damage and Antioxidant Defense in Ferroptosis
Kuang, F., Liu, J., Tang, D., & Kang, R. (2020) · Frontiers in Cell and Developmental Biology · doi:10.3389/fcell.2020.586578 · Cited by 531
Metadata
- Authors
- Chen, X., Xu, S., Zhao, C., & Liu, B.
- Venue
- Biochemical and Biophysical Research Communications
- Publisher
- Elsevier BV
- Published
- 2019-08
- Volume
- 516
- Issue
- 1
- Pages
- 37-43
- ISSN
- 0006-291X (ISSN-L)
- OpenAlex
- W2950662228
- Cited by
- 258
- References
- 31
- FWCI
- 17.88
- Type
- journal article
- Language
- en
- Open access
- closed
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- Chen, X., Xu, S., Zhao, C., & Liu, B. (2019). Role of TLR4/NADPH oxidase 4 pathway in promoting cell death through autophagy and ferroptosis during heart failure. Biochemical and Biophysical Research Communications. https://doi.org/10.1016/j.bbrc.2019.06.015
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