eISSN: 1644-4124
ISSN: 1426-3912
Central European Journal of Immunology
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2/2024
vol. 49
 
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Editor’s Pick

Exploring the role of hyperforin in modulating the NF-κB/miR-21 axis in sepsis-induced acute kidney injury

Paulina Niedźwiedzka-Rystwej
1, 2
,
Dorota Siwicka
3
,
Andrzej Eljaszewicz
4

  1. Institute of Biology, University of Szczecin, Szczecin, Poland
  2. Centre for Experimental Immunology and Immunobiology in Infectious Disease and Cancer, University of Szczecin, Szczecin, Poland
  3. Department of Anaesthesiology and Intensive Care, Medical University in Lublin, Lublin, Poland
  4. Centre of Regenerative Medicine, Medical University of Bialystok, Bialystok, Poland
Cent Eur J Immunol 2024; 49 (2): 91
Online publish date: 2024/08/26
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Acute kidney injury, previously called acute renal failure, is a severe and sudden decrease in kidney function [1]. Sepsis is one of the leading causes of acute kidney injury, especially in critically ill patients, as a consequence of inflammatory response and direct nephrotoxic and ischaemic processes [2-4]. The development of acute kidney injury during sepsis significantly increases morbidity and mortality in this group of patients [5]. Despite advances in critical care, effective therapeutic options for sepsis-induced acute kidney injury remain challenging, prompting an ongoing search for novel interventions. The study published in this issue of the Central European Journal of Immunology by Haozhe Fan and collaborators on hyperforin (HYP) offers evidence for its potential role in mitigating inflammation and protecting renal function [6].

Hyperforin, a bioactive compound derived from Hypericum perforatum (St. John’s Wort), has been previously recognised for its therapeutic potential [7-10]. The study of Haozhe Fan and collaborators extends these findings by exploring the pharmacological effects of HYP on lipopolysaccharide (LPS)-induced inflammation and subsequent acute kidney injury in both in vitro and in vivo septic models. The researchers administered HYP to LPS-stimulated podocytes and LPS-injected mice, significantly reducing podocyte apoptosis and renal injury.

The study’s findings are particularly noteworthy for elucidating the potential mechanism of action of HYP. HYP was observed to inhibit the NF-κB signalling pathway. Specifically, HYP was shown to hinder the LPS-induced transactivation of miR-21 by NF-κB signalling. The excessive activation of the NF-κB/miR-21 axis was found to contribute to the inflammatory cascade, leading to podocyte apoptosis and renal injury. Conversely, HYP reduces podocyte apoptosis and ameliorates LPS-induced renal damage.

This study aligns with previous research published in the Central European Journal of Immunology that highlighted the importance of ncRNAs in acute kidney injury, such as the modulation of the lncRNA MALAT1/miR205 axis [11] and the downregulation of lncRNA NEAT1 [12], both of which have been shown to alleviate kidney damage. Mechanisms of regulation and kidney repair in acute kidney injury have been subjects of recent research, especially in critical illness [13].

References

1 

KDIGO AKI Work Group (2012): KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl 2: 1-138.

2 

Kellum JA, Romagnani P, Ashuntantang G, et al. (2021): Acute kidney injury. Nat Rev Dis Primers 7: 52.

3 

Jiang W, Song L, Zhang Y, et al. (2024): The influence of gender on the epidemiology of and outcome from sepsis associated acute kidney injury in ICU: a retrospective propensity-matched cohort study. Eur J Med Res 17: 29-56.

4 

Hoste EA, Bagshaw SM, Bellomo R, et al. (2015): Epidemiology of acute kidney injury in critically ill patients: the multinational AKI-EPI study. Intensive Care Med 41: 1411-1423.

5 

Kellum JA, Lameire N, KDIGO AKI Guideline Work Group (2013): Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care (London, England) 17: 204.

6 

Fan H, He X, Tong H, Chen K (2024): Preventive effect of hyperforin on lipopolysaccharide-induced acute kidney injury and inflammation by repressing the NF-κB/miR-21 axis. Cent Eur J Immunol 49: 169-186.

7 

Novelli M, Beffy P, Menegazzi M, et al. (2014): St. John’s wort extract and hyperforin protect rat and human pancreatic islets against cytokine toxicity. Acta Diabetol 51: 113-121.

8 

Chen WT, Chen YK, Lin SS, Hsu FT (2018): Hyperforin suppresses tumor growth and NF-κB-mediated anti-apoptotic and invasive potential of non-small cell lung cancer. Anticancer Res 38: 2161-2167.

9 

Novelli M, Menegazzi M, Beffy P, et al. (2016): St. John’s wort extract and hyperforin inhibit multiple phosphorylation steps of cytokine signaling and prevent inflammatory and apoptotic gene induction in pancreatic β cells. Int J Biochem Cell Biol 81: 92-104.

10 

Li XX, Yan Y, Zhang J, et al. (2023): Hyperforin: A natural lead compound with multiple pharmacological activities. Phytochemistry 206: 113526.

11 

Wang B, Wang Y, Xu K, et al. (2021): Resveratrol alleviates sepsis-induced acute kidney injury by deactivating the lncRNA MALAT1/MiR-205 axis. Cent Eur J Immunol 46: 295-304.

12 

Zhou Y, Wang Y, Li Q, et al. (2022): Downregulation of lnc-RNA NEAT1 alleviates sepsis-induced acute kidney injury. Cent Eur J Immunol 47: 8-19.

13 

Pickkers P, Angus DC, Bass K, et al. (2024): Phase-3 trial of recombinant human alkaline phosphatase for patients with sepsis-associated acute kidney injury (REVIVAL). Intensive Care Med 50: 68-78.

Copyright: © 2024 Polish Society of Experimental and Clinical Immunology This is an Open Access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) License (http://creativecommons.org/licenses/by-nc-sa/4.0/), allowing third parties to copy and redistribute the material in any medium or format and to remix, transform, and build upon the material, provided the original work is properly cited and states its license.
 
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