Antioxidant System Efficiency in Kidney Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 June 2024 | Viewed by 1224

Special Issue Editors


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Guest Editor
1. Carlos Chagas Filho Institute of Biophysics, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
2. National Center of Structural Biology and Bioimaging, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil
Interests: kidney; acute and chronic kidney disease; vasoactive peptides; renal oxidative stress; cell therapy; extracellular vesicles; biophysics of membrane transport
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Guest Editor
Institute of Biomedical Sciences, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil
Interests: kidney; acute and chronic kidney disease

Special Issue Information

Dear Colleagues,

Acute and chronic renal diseases are severe illnesses of significant incidence in which dialysis and transplantation are frequently the only therapeutic options. These options do not avoid fatal outcomes. Chronic renal diseases and their end-stage frequently follow acute episodes. Notably, there are no efficient and specific treatments, which is why dialysis and transplantation are the only therapeutic options at the moment.

Tissue oxidative stress is a critical physiopathological component of renal lesions of many different origins. The intense oxidative metabolism of kidney tissue, especially in the cortex, favors the formation of reactive oxygen species. Due to this critical pathophysiological component, the search for antioxidant agents has recently intensified. At the same time, understanding oxidizing mechanisms and antioxidants has become imperative for a careful search for new agents and products of the most diverse origins.

There are two primary sources of reactive oxygen species capable of causing kidney damage, mitochondrial and extramitochondrial, and there is often crosstalk between them. The central oxidizing species is the superoxide anion, but different cycles can lead to other species, such as oxydryl radical. Thus, antioxidant systems—enzymatic or not—are found within both the mitochondria of the renal cortex and the medulla. They are the target of research to obtain new drugs and products, including natural products and their derivatives, and many forms of medicinal chemistry. Antioxidant products are also encountered in the new field of regenerative medicine.

This Special Issue of Antioxidants aims to stimulate the sharing of new results and ideas in the field of oxidant and antioxidant mechanisms in different segments of kidney tissue, opening up new avenues of knowledge for preventing and treating kidney diseases.

Prof. Dr. Adalberto Vieyra
Dr. Lucienne S. Lara
Guest Editors

Manuscript Submission Information

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Keywords

  • antioxidants
  • acute renal diseases
  • renal ischemia and reperfusion
  • chronic renal diseases
  • renal oxidative stress
  • mitochondria
  • antioxidant enzymes
  • renal renin–angiotensin–aldosterone and oxidative stress
  • hypertension and renal oxidative stress

Published Papers (1 paper)

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Research

16 pages, 6507 KiB  
Article
Liproxstatin-1 Alleviated Ischemia/Reperfusion-Induced Acute Kidney Injury via Inhibiting Ferroptosis
by Zhiyuan Shi, Yifan Du, Jianzhong Zheng, Wenbin Tang, Qing Liang, Zeyuan Zheng, Bin Liu, Huimin Sun, Kejia Wang and Chen Shao
Antioxidants 2024, 13(2), 182; https://doi.org/10.3390/antiox13020182 - 31 Jan 2024
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Abstract
Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal [...] Read more.
Ferroptosis, as a novel regulable cell death, is characterized by iron overload, glutathione depletion, and an accumulation of lipid peroxides. Recently, it has been discovered that ferroptosis is involved in ischemia/reperfusion (I/R)-induced acute kidney injury (AKI) and plays a crucial role in renal tubular cell death. In this study, we tried to investigate the effect and mechanism of liproxstatin-1 (Lip-1) in I/R-induced AKI and seek the key regulator of ferroptosis in I/R-induced AKI. Mice were administrated with clamping bilateral renal pedicles for 30 min. We found that early growth response 1 (EGR1) might be a key regulator of ferroptosis, and Lip-1 could suppress ferroptosis via EGR1. Meanwhile, Lip-1 could reduce macrophage recruitment and the release of inflammatory cytokines. These findings indicated that Lip-1 alleviated I/R-induced AKI via regulating EGR1, and it might pave the theoretical basis of a new therapeutic strategy for I/R-induced AKI. Full article
(This article belongs to the Special Issue Antioxidant System Efficiency in Kidney Diseases)
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