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Reactive oxygen species modulator 1 regulates oxidative stress and induces renal and pulmonary fibrosis in a unilateral ureteral obstruction rat model and in HK-2 cells.

Authors: Liu, Donghai  Liu, Ying  Xia, Zhenkun  Dong, Haiyun  Yi, Zhuwen 
Citation: Liu D, etal., Mol Med Rep. 2017 Oct;16(4):4855-4862. doi: 10.3892/mmr.2017.7161. Epub 2017 Aug 3.
Pubmed: (View Article at PubMed) PMID:28791399
DOI: Full-text: DOI:10.3892/mmr.2017.7161

Renal interstitial fibrosis (RIF) is the main process that leads to renal failure. It is necessary to investigate the mechanism of RIF and identify appropriate methods of regulating it. Furthermore, unilateral ureteral obstruction is a frequently used model for the study of RIF. The morphological damage associated with kidney and lung dysfunction was detected using histopathological experiments. Subsequently, high expression of reactive oxygen species (ROS) modulator 1 (ROMO1) and ROS was measured in blood serum. In addition, epithelial-mesenchymal transition marker, transforming growth factor ß (TGF-ß) and mothers against decapentaplegic homolog 2/3 expression was evaluated using the reverse transcription-quantitative polymerase chain reaction and western blotting. All serious symptoms were relieved to a certain extent following oxidation inhibitor intervention using three common antioxidants. HK-2 cells were treated with H2O2 to cause oxidative stress, and ROMO1 and fibrosis marker expression increased; however, activation was suppressed byROMO1 knockout. The present study provides evidence that the expression of ROMO1 induces ROS production and activates the TGF-ß signaling pathway. It may be concluded that ROMO1 helps to provide a molecular basis for improved clinical intervention and prognosis of patients.

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RGD Object Information
RGD ID: 13463462
Created: 2017-12-15
Species: All species
Last Modified: 2017-12-15
Status: ACTIVE



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RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.