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Article

Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis

by
Corina Daniela Ene
1,*,
Simona Roxana Georgescu
2,*,
Mircea Tampa
3,*,
Clara Matei
4,
Cristina Iulia Mitran
5,
Madalina Irina Mitran
5,
Mircea Nicolae Penescu
1,6 and
Ilinca Nicolae
2
1
Department of Nephrology, Davila Clinical Hospital of Nephrology, 010731 Bucharest, Romania
2
Department of Dermatology, Victor Babes Clinical Hospital of Tropical and Infectious Diseases, 030303 Bucharest, Romania
3
Department of Dermatology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
4
Department of Dermatology, Colentina Clinical Hospital, 020125 Bucharest, Romania
5
Department of Microbiology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
6
Department of Nephrology, Carol Davila University of Medicine and Pharmacy, 020021 Bucharest, Romania
*
Authors to whom correspondence should be addressed.
J. Pers. Med. 2021, 11(8), 693; https://doi.org/10.3390/jpm11080693
Submission received: 22 June 2021 / Revised: 18 July 2021 / Accepted: 19 July 2021 / Published: 22 July 2021
(This article belongs to the Special Issue Personalized Medicine in the Field of Inflammatory Skin Disorders)
Versions Notes

Abstract

The interaction of reactive oxygen species (ROS) with lipids, proteins, nucleic acids and hydrocarbonates promotes acute and chronic tissue damage, mediates immunomodulation and triggers autoimmunity in systemic lupus erythematous (SLE) patients. The aim of the study was to determine the pathophysiological mechanisms of the oxidative stress-related damage and molecular mechanisms to counteract oxidative stimuli in lupus nephritis. Our study included 38 SLE patients with lupus nephritis (LN group), 44 SLE patients without renal impairment (non-LN group) and 40 healthy volunteers as control group. In the present paper, we evaluated serum lipid peroxidation, DNA oxidation, oxidized proteins, carbohydrate oxidation, and endogenous protective systems. We detected defective DNA repair mechanisms via 8-oxoguanine-DNA-glycosylase (OGG1), the reduced regulatory effect of soluble receptor for advanced glycation end products (sRAGE) in the activation of AGE-RAGE axis, low levels of thiols, disulphide bonds formation and high nitrotyrosination in lupus nephritis. All these data help us to identify more molecular mechanisms to counteract oxidative stress in LN that could permit a more precise assessment of disease prognosis, as well as developing new therapeutic targets.
Keywords: systemic lupus erythematous; lupus nephritis; lipid peroxidation; DNA oxidation; oxidized proteins; carbohydrate oxidation; antioxidative stress strategies; biomarkers systemic lupus erythematous; lupus nephritis; lipid peroxidation; DNA oxidation; oxidized proteins; carbohydrate oxidation; antioxidative stress strategies; biomarkers

Share and Cite

MDPI and ACS Style

Ene, C.D.; Georgescu, S.R.; Tampa, M.; Matei, C.; Mitran, C.I.; Mitran, M.I.; Penescu, M.N.; Nicolae, I. Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis. J. Pers. Med. 2021, 11, 693. https://doi.org/10.3390/jpm11080693

AMA Style

Ene CD, Georgescu SR, Tampa M, Matei C, Mitran CI, Mitran MI, Penescu MN, Nicolae I. Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis. Journal of Personalized Medicine. 2021; 11(8):693. https://doi.org/10.3390/jpm11080693

Chicago/Turabian Style

Ene, Corina Daniela, Simona Roxana Georgescu, Mircea Tampa, Clara Matei, Cristina Iulia Mitran, Madalina Irina Mitran, Mircea Nicolae Penescu, and Ilinca Nicolae. 2021. "Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis" Journal of Personalized Medicine 11, no. 8: 693. https://doi.org/10.3390/jpm11080693

APA Style

Ene, C. D., Georgescu, S. R., Tampa, M., Matei, C., Mitran, C. I., Mitran, M. I., Penescu, M. N., & Nicolae, I. (2021). Cellular Response against Oxidative Stress, a Novel Insight into Lupus Nephritis Pathogenesis. Journal of Personalized Medicine, 11(8), 693. https://doi.org/10.3390/jpm11080693

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