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논문분류	춘계학술대회 초록집
제목	Glutamyl-prolyl-tRNA-synthetase 1 regulates kidney fibrosis by controlling STAT3 and mitochondrial dysfunction
저자	Seung Seob Son
출판정보	2023; 2023(1):
키워드
초록	Objectives: Glutamyl-prolyl-tRNA synthetase 1 (EPRS1), an enzyme necessary for synthesizing proline-rich profibrotic proteins such as collagen, is known to be involved in various fibrotic diseases. This study aims to identify the results of the genetic deletion of EPRS1 andprove that EPRS1 can be involved in kidney fibrosis. Methods: To examine the kidney effects of EPRS1 inhibition, we used folic acid (FA)-induced chronic kidney disease (CKD) model in EPRS1 heterozygous knockout (C57BL/6 EPRS1tm1b, Eprs1+/-) mice and wild-type mice. Additionally, we tested EPRS1 inhibition genetically in HK-2 cells to determine if it played a role in fibrosis inhibition and mitochondrial dysfunction. Results: FA-induced kidney fibrosis, mitochondrial dysfunction, increased blood urea nitrogen and serum creatinine, and upregulated EPRS1 expression were observed in wild-type CKD mice. Eprs1+/- mice decreased EPRS1 levels, kidney fibrosis, and mitochondrial dysfunction. Moreover, Eprs1+/- mice effectively inhibited both extracellular matrix marker (Collagen 1A1) and the levels of SIRT1/STAT3. Similarly, the genetic inhibition of EPRS1 in transforming growth factor-β1-induced HK-2 cells inhibited fibrosis by suppressing p-STAT3 and activating SIRT1/PGC-1α and improving mitochondrial dysfunction. Similarly, the genetic inhibition of EPRS1 in transforming growth factor-β1-induced HK-2 cells inhibited fibrosis by suppressing p-STAT3 and activating SIRT1/PGC-1α. Genetic inhibition of EPRS1 also improved mitochondrial dysfunction. Conclusions: Our results indicate for the first time an increased expression of EPRS1 in kidney fibrosis and that EPRS1 inhibition could be effective by regulating mitochondrial dysfunction and p-STAT3 signaling in chronic kidney disease.
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