PMID- 35164031 OWN - NLM STAT- MEDLINE DCOM- 20220225 LR - 20220225 IS - 1420-3049 (Electronic) IS - 1420-3049 (Linking) VI - 27 IP - 3 DP - 2022 Jan 25 TI - Anti-Fibrotic Effect of Synthetic Noncoding Oligodeoxynucleotide for Inhibiting mTOR and STAT3 via the Regulation of Autophagy in an Animal Model of Renal Injury. LID - 10.3390/molecules27030766 [doi] LID - 766 AB - Renal fibrosis is a common process of various kidney diseases. Autophagy is an important cell biology process to maintain cellular homeostasis. In addition, autophagy is involved in the pathogenesis of various renal disease, including acute kidney injury, glomerular diseases, and renal fibrosis. However, the functional role of autophagy in renal fibrosis remains poorly unclear. The mammalian target of rapamycin (mTOR) plays a negative regulatory role in autophagy. Signal transducer and activator of transcription 3 (STAT3) is an important intracellular signaling that may regulate a variety of inflammatory responses. In addition, STAT3 regulates autophagy in various cell types. Thus, we synthesized the mTOR/STAT3 oligodeoxynucleotide (ODN) to regulate the autophagy. The aim of this study was to investigate the beneficial effect of mTOR/STAT3 ODN via the regulation of autophagy appearance on unilateral ureteral obstruction (UUO)-induced renal fibrosis. This study showed that UUO induced inflammation, tubular atrophy, and tubular interstitial fibrosis. However, mTOR/STAT3 ODN suppressed UUO-induced renal fibrosis and inflammation. The autophagy markers have no statistically significant relation, whereas mTOR/STAT3 ODN suppressed the apoptosis in tubular cells. These results suggest the possibility of mTOR/STAT3 ODN for preventing renal fibrosis. However, the role of mTOR/STAT3 ODN on autophagy regulation needs to be further investigated. FAU - Jung, Hyun Jin AU - Jung HJ AD - Department of Urology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - An, Hyun-Jin AU - An HJ AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Gwon, Mi-Gyeong AU - Gwon MG AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Gu, Hyemin AU - Gu H AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Bae, Seongjae AU - Bae S AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Lee, Sun-Jae AU - Lee SJ AUID- ORCID: 0000-0002-8552-6049 AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Kim, Young-Ah AU - Kim YA AUID- ORCID: 0000-0001-7850-5509 AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Leem, Jaechan AU - Leem J AUID- ORCID: 0000-0003-2329-4374 AD - Department of Immunology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. FAU - Park, Kwan-Kyu AU - Park KK AD - Department of Pathology, College of Medicine, Catholic University of Daegu, Daegu 42472, Korea. LA - eng GR - NRF-2019R1G1A1010882/National Research Foundation of Korea/ PT - Journal Article DEP - 20220125 PL - Switzerland TA - Molecules JT - Molecules (Basel, Switzerland) JID - 100964009 RN - 0 (Oligodeoxyribonucleotides) RN - 0 (STAT3 Transcription Factor) RN - EC 2.7.11.1 (TOR Serine-Threonine Kinases) SB - IM MH - Animals MH - Autophagy/*drug effects MH - Disease Models, Animal MH - Fibrosis/*prevention & control MH - Kidney/*injuries MH - Oligodeoxyribonucleotides/*antagonists & inhibitors MH - STAT3 Transcription Factor/*metabolism MH - TOR Serine-Threonine Kinases/*metabolism PMC - PMC8840279 OTO - NOTNLM OT - STAT3 OT - antisense OT - autophagy OT - decoy OT - mTOR OT - oligodeoxynucleotide OT - renal fibrosis COIS- The authors declare no conflict of interest. EDAT- 2022/02/16 06:00 MHDA- 2022/02/26 06:00 PMCR- 2022/01/25 CRDT- 2022/02/15 01:19 PHST- 2021/12/14 00:00 [received] PHST- 2022/01/10 00:00 [revised] PHST- 2022/01/19 00:00 [accepted] PHST- 2022/02/15 01:19 [entrez] PHST- 2022/02/16 06:00 [pubmed] PHST- 2022/02/26 06:00 [medline] PHST- 2022/01/25 00:00 [pmc-release] AID - molecules27030766 [pii] AID - molecules-27-00766 [pii] AID - 10.3390/molecules27030766 [doi] PST - epublish SO - Molecules. 2022 Jan 25;27(3):766. doi: 10.3390/molecules27030766.