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

被引：29

作者：

Ene, Corina Daniela ^{[1
]}

Georgescu, Simona Roxana ^{[2
]}

Tampa, Mircea ^{[3
]}

Matei, Clara ^{[4
]}

Mitran, Cristina Iulia ^{[5
]}

Mitran, Madalina Irina ^{[5
]}

Penescu, Mircea Nicolae ^{[1
,6
]}

Nicolae, Ilinca ^{[2
]}

机构：

[1] Davila Clin Hosp Nephrol, Dept Nephrol, Bucharest 010731, Romania

[2] Victor Babes Clin Hosp Trop & Infect Dis, Dept Dermatol, Bucharest 030303, Romania

[3] Carol Davila Univ Med & Pharm, Dept Dermatol, Bucharest 020021, Romania

[4] Colentina Clin Hosp, Dept Dermatol, Bucharest 020125, Romania

[5] Carol Davila Univ Med & Pharm, Dept Microbiol, Bucharest 020021, Romania

[6] Carol Davila Univ Med & Pharm, Dept Nephrol, Bucharest 020021, Romania

来源：

JOURNAL OF PERSONALIZED MEDICINE | 2021年 / 11卷 / 08期

关键词：

systemic lupus erythematous; lupus nephritis; lipid peroxidation; DNA oxidation; oxidized proteins; carbohydrate oxidation; antioxidative stress strategies; biomarkers; GLYCATION END-PRODUCTS; SOLUBLE RECEPTOR; DISEASE-ACTIVITY; ERYTHEMATOSUS PATIENTS; PROTEIN OXIDATION; PLASMA-LEVEL; SERUM-LEVELS; SEVERITY; MARKERS; RAGE;

D O I：

10.3390/jpm11080693

中图分类号：

R19 [保健组织与事业（卫生事业管理）];

学科分类号：

摘要：

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.

引用

页数：18

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