The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
Targeting the transcription factor Nrf2 to ameliorate oxidative stress and inflammation in chronic kidney disease
Open accessAbstract
Oxidative stress and inflammation are mediators in the development and progression of chronic kidney disease (CKD) and its complications, and they are inseparably linked as each begets and amplifies the other. CKD-associated oxidative stress is due to increased production of reactive oxygen species (ROS) and diminished antioxidant capacity. The latter is largely caused by impaired activation of Nrf2, the transcription factor that regulates genes encoding antioxidant and detoxifying molecules. Protective effects of Nrf2 are evidenced by amelioration of oxidative stress, inflammation, and kidney disease in response to natural Nrf2 activators in animal models, while Nrf2 deletion amplifies these pathogenic pathways and leads to autoimmune nephritis. Given the role of impaired Nrf2 activity in CKD-induced oxidative stress and inflammation, interventions aimed at restoring Nrf2 may be effective in retarding CKD progression. Clinical trials of the potent Nrf2 activator bardoxolone methyl showed significant improvement in renal function in CKD patients with type 2 diabetes. Results of the ongoing BEACON trial investigating the effect of this drug on time to end-stage renal disease or cardiovascular death will help further characterize the efficacy of Nrf2 pharmacological modulation in CKD. This article provides an overview of the role of impaired Nrf2 activity in the pathogenesis of CKD-associated oxidative stress and inflammation and the potential utility of targeting Nrf2 in the treatment of CKD.
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Cites
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Cited by
Targeting the KEAP1-NRF2 system to prevent kidney disease progression
Nezu, M., Suzuki, N., & Yamamoto, M. (2017) · American Journal of Nephrology · doi:10.1159/000475890 · Cited by 3,447
Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment
Samsu, N. (2021) · BioMed Research International · doi:10.1155/2021/1497449 · Cited by 1,001
Oxidative Stress in Human Pathology and Aging: Molecular Mechanisms and Perspectives
Hajam, Y. A., Rani, R., Ganie, S. Y., Sheikh, T. A., Javaid, D., Qadri, S. S., Pramodh, S., Alsulimani, A., Alkhanani, M. F., Harakeh, S., et al. (2022) · Cells · doi:10.3390/cells11030552 · Cited by 915
Diabetic nephropathy – complications and treatment
Lim, A. (2014) · International Journal of Nephrology and Renovascular Disease · doi:10.2147/ijnrd.s40172 · Cited by 583
AKI on CKD: heightened injury, suppressed repair, and the underlying mechanisms
He, L., Wei, Q., Liu, J., Yi, M., Liu, Y., Liu, H., Sun, L., Peng, Y., Liu, F., Venkatachalam, M. A., et al. (2017) · Kidney International · doi:10.1016/j.kint.2017.06.030 · Cited by 448
Metadata
- Authors
- Ruiz, S., Pergola, P. E., Zager, R. A., & Vaziri, N. D.
- Venue
- Kidney International
- Publisher
- Elsevier BV
- Published
- 2013-06
- Volume
- 83
- Issue
- 6
- Pages
- 1029-1041
- ISSN
- 0085-2538 (ISSN-L)
- OpenAlex
- W2031004071
- Cited by
- 718
- References
- 19
- FWCI
- 19.37
- Type
- journal article
- Language
- en
- Open access
- bronze
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