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HOME > Kosin Med J > Volume 38(3); 2023 > Article
Editorial
Omega-3 fatty acids: promising therapeutic agents for combating kidney injuries
Hee-Jae Chaorcid
Kosin Medical Journal 2023;38(3):157-158.
DOI: https://doi.org/10.7180/kmj.23.135
Published online: September 7, 2023

Department of Parasitology and Genetics, Institute for Medical Science, Kosin University College of Medicine, Busan, Korea

Corresponding Author: Hee-Jae Cha, PhD Department of Parasitology and Genetics, Kosin University College of Medicine, 262 Gamcheon-ro, Seo-gu, Busan 49267, Korea Tel: +82-51-990-6428 Fax: +82-51-990-3081 E-mail: hcha@kosin.ac.kr
• Received: July 3, 2023   • Revised: July 17, 2023   • Accepted: August 7, 2023

Copyright © 2023 Kosin University College of Medicine.

This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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See the article "Omega-3 fatty acids upregulate Nrf2 expression and attenuate apoptosis, inflammation, and fibrosis in a rat model of cyclosporine-induced nephropathy" on page 184.
Cyclosporine (CsA)-induced nephropathy is a debilitating condition characterized by renal dysfunction accompanied by inflammation, apoptosis, fibrosis, and hypoxic injury [1]. Despite extensive research, the influence of omega-3 fatty acids (O-3FA) on nuclear factor erythroid 2-related factor 2 (Nrf2) expression, a key regulator of cellular defense mechanisms, remains unclear [2,3]. However, a recent groundbreaking study sheds light on the potential benefits of O-3FA for attenuating these harmful processes in a rat model of CsA-induced nephropathy [4].
The study divided male Sprague-Dawley rats into three groups: a control group, a group treated with CsA, and a group treated with both CsA and O-3FA. The researchers observed significant kidney function impairment in the CsA-treated rats compared to the control group. Additionally, markers associated with apoptosis, such as caspase-3, caspase-7, and the Bax to Bcl2 ratio, were activated in the CsA-treated group. Remarkably, O-3FA supplementation attenuated these apoptotic activation patterns, indicating its potential anti-apoptotic effects.
Furthermore, the CsA-treated group exhibited increased expression of the inflammatory marker ED-1 and inhibition of the IĸB protein. However, O-3FA supplementation effectively mitigated the inflammatory response, as evidenced by the reduced expression of ED-1 and IĸB. Furthermore, CsA treatment led to the activation of Smad2/3, Smad4, and transforming growth factor-β1, all associated with renal fibrosis. Nevertheless, O-3FA prevented these activations, highlighting its potential anti-fibrotic properties.
Interestingly, the researchers discovered that Nrf2 expression was decreased in CsA-treated rats, but supplementation with O-3FA significantly increased its expression. This finding suggests that Nrf2 may act as a potential mediator induced by O-3FA supplementation, playing a crucial role in attenuating pro-inflammatory pathways, fibrotic processes, and apoptosis.
The study provides compelling evidence that O-3FA supplementation holds immense promise as a therapeutic intervention in CsA-induced nephropathy. By upregulating Nrf2 expression, O-3FA exhibits notable anti-inflammatory, anti-apoptotic, and anti-fibrotic effects, ultimately protecting the kidneys from damage. However, further investigations are necessary to elucidate the intricate crosstalk between Nrf2 expression and the signaling pathways involved in O-3FA treatment.
These findings offer new insights into the potential mechanisms underlying the protective effects of O-3FA against kidney injuries. If translated into clinical practice, O-3FA supplementation could emerge as a valuable adjunct therapy for patients with CsA-induced nephropathy, helping to alleviate their symptoms and enhance renal function. Nonetheless, additional studies are warranted to fully understand the therapeutic potential and optimize the dosing and administration strategies of O-3FA in human subjects.
It would be premature to conclude that the efficacy of O-3FA has been proven based solely on the content of this manuscript. One limitation of this study is that it was conducted on male Sprague-Dawley rats, which may not fully represent the response to O-3FA supplementation in humans. Animal models do not always perfectly reflect human physiology, and there may be species-specific differences in the effects of O-3FA on Nrf2 expression and its associated pathways. Furthermore, the authors acknowledged the need for further studies to elucidate the crosstalk between Nrf2 expression and signals related to O-3FA treatment. This study does not provide a comprehensive understanding of the underlying mechanisms by which O-3FA influences Nrf2 and its downstream effects. Future research is necessary to fully explore and confirm these relationships.
In conclusion, despite some limitations, this study marks a significant advancement in our understanding of the protective effects of O-3FA against CsA-induced nephropathy [5]. With further exploration and clinical validation, O-3FA could become an integral component of the treatment arsenal, offering hope to patients suffering from this challenging kidney condition.

Conflicts of interest

No potential conflict of interest relevant to this article was reported.

Funding

None.

Author contributions

All work was performed by HJC.

  • 1. Patocka J, Nepovimova E, Kuca K, Wu W. Cyclosporine A: chemistry and toxicity. A review. Curr Med Chem 2021;28:3925–34.ArticlePubMed
  • 2. Shin DH, Park HM, Jung KA, Choi HG, Kim JA, Kim DD, et al. The NRF2-heme oxygenase-1 system modulates cyclosporin A-induced epithelial-mesenchymal transition and renal fibrosis. Free Radic Biol Med 2010;48:1051–63.ArticlePubMedPMC
  • 3. Ishikado A, Morino K, Nishio Y, Nakagawa F, Mukose A, Sono Y, et al. 4-Hydroxy hexenal derived from docosahexaenoic acid protects endothelial cells via Nrf2 activation. PLoS One 2013;8:e69415.ArticlePubMedPMC
  • 4. An WS, Kim HJ, Cho KH, Vaziri ND. Omega-3 fatty acid supplementation attenuates oxidative stress, inflammation, and tubulointerstitial fibrosis in the remnant kidney. Am J Physiol Renal Physiol 2009;297:F895–903.ArticlePubMed
  • 5. Lee JY, Son YK, Lee MH, Lee SM, Kim SE, An WS. Omega-3 fatty acids upregulate Nrf2 expression and attenuate apoptosis, inflammation, and fibrosis in a rat model of cyclosporine-induced nephropathy. Kosin Med J 2023;38:184–92.Article

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