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Renal Disorders Related to Oxidative Stress: From Physiology to Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (20 December 2022) | Viewed by 11073

Special Issue Editor

Special Issue Information

Dear Colleagues,

Oxidative stress, as a mechanism underlying many clinical conditions, is well known to play a crucial role in the development of renal disease as well as cardiovascular disease, diabetes, and cancers. However, the complex associations of oxidative status with hormones and inflammation are still far from being completely understood, since reciprocal and opposite influences can be exerted between these pathogenic factors. In addition, various nuclear factors and receptors involved in the regulation of antioxidant defense, nitric oxide production, inflammation, energy, and/or iron metabolism provide new targets for the prevention and treatment of renal disease and comorbid diseases.

Recent data have demonstrated that natural antioxidants can modulate oxidative stress and improve immune function. Thus, the role of compounds with antioxidant properties that promote health and counteract oxidative stress in the renal disease is worth investigating further. An exhaustive understanding of the role of the involvement of antioxidants in redox modulation would be useful for potential interventions and, subsequently, promoting health.

Therefore, we aim to publish a Special Issue which can cover a wide spectrum, from biological to translational studies, in the field of renal disorders.

This Special Issue will gather reviews and original data that focus on defining the following:

  • Abnormalities in the antioxidant system in patients with renal diseases;
  • Antioxidant therapeutics;
  • Biomarkers and diagnostic methods in oxidative stress.

Dr. Keiko Hosohata
Guest Editor

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Keywords

  • reactive oxygen species (ROS)
  • inflammation
  • metabolic syndrome
  • antioxidant response
  • redox balance
  • aging
  • proinflammatory signals
  • kidney

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Published Papers (3 papers)

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Research

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14 pages, 4801 KiB  
Article
β-Cryptoxanthin Maintains Mitochondrial Function by Promoting NRF2 Nuclear Translocation to Inhibit Oxidative Stress-Induced Senescence in HK-2 Cells
by Ye Zhang, Hu Mao, Yanze Li, Yufeng Xiong, Xiuheng Liu, Lei Wang and Zhiyuan Chen
Int. J. Mol. Sci. 2023, 24(4), 3851; https://doi.org/10.3390/ijms24043851 - 14 Feb 2023
Cited by 4 | Viewed by 2167
Abstract
The mechanisms of acute kidney injury and chronic kidney disease remain incompletely revealed, and drug development is a pressing clinical challenge. Oxidative stress-induced cellular senescence and mitochondrial damage are important biological events in a variety of kidney diseases. As a type of carotenoid, [...] Read more.
The mechanisms of acute kidney injury and chronic kidney disease remain incompletely revealed, and drug development is a pressing clinical challenge. Oxidative stress-induced cellular senescence and mitochondrial damage are important biological events in a variety of kidney diseases. As a type of carotenoid, β-Cryptoxanthin (BCX) has various biological functions, which means it is a potential therapeutic candidate for the treatment of kidney disease. However, the role of BCX in the kidney is unclear, and the effect of BCX on oxidative stress and cellular senescence in renal cells is also unknown. Therefore, we conducted a series of studies on human renal tubular epithelial (HK-2) cells in vitro. In the present study, we investigated the effect of BCX pretreatment on H2O2-induced oxidative stress and cellular senescence and explored the potential mechanism of BCX action. The results showed that BCX attenuated H2O2-induced oxidative stress and cellular senescence in HK-2 cells. Moreover, BCX promoted NRF2 nuclear expression, maintained mitochondrial function, and reduced mitochondrial damage in HK-2 cells. In addition, silencing NRF2 altered the protective effect of BCX on mitochondria and significantly reversed the anti-oxidative stress and anti-senescence effects of BCX in HK-2 cells. We concluded that BCX maintained mitochondrial function by promoting NRF2 nuclear translocation to inhibit oxidative stress-induced senescence in HK-2 cells. In light of these findings, the application of BCX might be a promising strategy for the prevention and treatment of kidney diseases. Full article
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10 pages, 2075 KiB  
Article
In Vivo and In Vitro Evaluation of Urinary Biomarkers in Ischemia/Reperfusion-Induced Kidney Injury
by Keiko Hosohata, Denan Jin and Shinji Takai
Int. J. Mol. Sci. 2021, 22(21), 11448; https://doi.org/10.3390/ijms222111448 - 23 Oct 2021
Cited by 15 | Viewed by 3002
Abstract
Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker [...] Read more.
Oxidative stress plays an important role in the pathophysiology of acute kidney injury (AKI). Previously, we reported that vanin-1, which is involved in oxidative stress, is associated with renal tubular injury. This study was aimed to determine whether urinary vanin-1 is a biomarker for the early diagnosis of AKI in two experimental models: in vivo and in vitro. In a rat model of AKI, ischemic AKI was induced in uninephrectomized rats by clamping the left renal artery for 45 min and then reperfusing the kidney. On Day 1 after renal ischemia/reperfusion (I/R), serum creatinine (SCr) in I/R rats was higher than in sham-operated rats, but this did not reach significance. Urinary N-acetyl-β-D-glucosaminidase (NAG) exhibited a significant increase but decreased on Day 2 in I/R rats. In contrast, urinary vanin-1 significantly increased on Day 1 and remained at a significant high level on Day 2 in I/R rats. Renal vanin-1 protein decreased on Days 1 and 3. In line with these findings, immunofluorescence staining demonstrated that vanin-1 was attenuated in the renal proximal tubules of I/R rats. Our in vitro results confirmed that the supernatant from HK-2 cells under hypoxia/reoxygenation included significantly higher levels of vanin-1 as well as KIM-1 and NGAL. In conclusion, our results suggest that urinary vanin-1 might be a potential novel biomarker of AKI induced by I/R. Full article
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Review

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15 pages, 930 KiB  
Review
Macrophage Migration Inhibitory Factor (MIF) as a Stress Molecule in Renal Inflammation
by Yao-Zhong Kong, Qiyan Chen and Hui-Yao Lan
Int. J. Mol. Sci. 2022, 23(9), 4908; https://doi.org/10.3390/ijms23094908 - 28 Apr 2022
Cited by 21 | Viewed by 5089
Abstract
Renal inflammation is an initial pathological process during progressive renal injury regardless of the initial cause. Macrophage migration inhibitory factor (MIF) is a truly proinflammatory stress mediator that is highly expressed in a variety of both inflammatory cells and intrinsic kidney cells. MIF [...] Read more.
Renal inflammation is an initial pathological process during progressive renal injury regardless of the initial cause. Macrophage migration inhibitory factor (MIF) is a truly proinflammatory stress mediator that is highly expressed in a variety of both inflammatory cells and intrinsic kidney cells. MIF is released from the diseased kidney immediately upon stimulation to trigger renal inflammation by activating macrophages and T cells, and promoting the production of proinflammatory cytokines, chemokines, and stress molecules via signaling pathways involving the CD74/CD44 and chemokine receptors CXCR2, CXCR4, and CXCR7 signaling. In addition, MIF can function as a stress molecule to counter-regulate the immunosuppressive effect of glucocorticoid in renal inflammation. Given the critical position of MIF in the upstream inflammatory cascade, this review focuses on the regulatory role and molecular mechanisms of MIF in kidney diseases. The therapeutic potential of targeting MIF signaling to treat kidney diseases is also discussed. Full article
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