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REVIEW: Targeting Inflammation and Oxidative Stress as a Therapy for Ischemic Kidney Injury

N. V. Andrianova1,2, D. B. Zorov1,3,a*, and E. Y. Plotnikov1,3,4,a*

1Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia

2Faculty of Bioengineering and Bioinformatics, Lomonosov Moscow State University, 119991 Moscow, Russia

3Kulakov National Medical Research Center of Obstetrics, Gynecology and Perinatology, 117997 Moscow, Russia

4Sechenov First Moscow State Medical University, Institute of Molecular Medicine, 119991 Moscow, Russia

* To whom correspondence should be addressed.

Received July 7, 2020; Revised July 23, 2020; Accepted July 29, 2020
Inflammation and oxidative stress are the main pathological processes that accompany ischemic injury of kidneys and other organs. Based on this, these factors are often chosen as a target for treatment of acute kidney injury (AKI) in a variety of experimental and clinical studies. Note, that since these two components are closely interrelated during AKI development, substances that treat one of the processes often affect the other. The review considers several groups of promising nephroprotectors that have both anti-inflammatory and antioxidant effects. For example, many antioxidants, such as vitamins, polyphenolic compounds, and mitochondria-targeted antioxidants, not only reduce production of the reactive oxygen species in the cell but also modulate activity of the immune cells. On the other hand, immunosuppressors and non-steroidal anti-inflammatory drugs that primarily affect inflammation also reduce oxidative stress under some conditions. Another group of therapeutics is represented by hormones, such as estrogens and melatonin, which significantly reduce severity of the kidney damage through modulation of both these processes. We conclude that drugs with combined anti-inflammatory and antioxidant capacities are the most promising agents for the treatment of acute ischemic kidney injury.
KEY WORDS: ischemia/reperfusion, nephroprotection, reactive oxygen species, SkQ, glucocorticoids, cyclooxygenase-2

DOI: 10.1134/S0006297920120111