ReferenceID 5447
Sirtuin 3 Activation by Honokiol Decreases Unilateral Ureteral Obstruction-Induced Renal Inflammation and Fibrosis via Regulation of Mitochondrial Dynamics and the Renal NF-κBTGF-β1/Smad Signaling Pathway
Int J Mol Sci
Renal fibrosis is a common feature of all progressive chronic kidney diseases. Sirtuin 3(SIRT3) is one of the mitochondrial sirtuins, and plays a role in the regulation of mitochondrialbiogenesis, oxidative stress, fatty
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Record Fields
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- Reference Id
- 5447
- Evidence Id
- 22037
- Core Evidence Id
- 22037
- Source Reference Id
- 4150
- Herb2 Reference Id
- HBREF004947
- Subject Paper Key
- HBIN029531_31936371
- Pubmed Id
- 31936371
- Doi
- 10.3390/ijms21020402
- Paper Title
- Sirtuin 3 Activation by Honokiol Decreases Unilateral Ureteral Obstruction-Induced Renal Inflammation and Fibrosis via Regulation of Mitochondrial Dynamics and the Renal NF-κBTGF-β1/Smad Signaling Pathway
- Paper Abstract
- Renal fibrosis is a common feature of all progressive chronic kidney diseases. Sirtuin 3(SIRT3) is one of the mitochondrial sirtuins, and plays a role in the regulation of mitochondrialbiogenesis, oxidative stress, fatty acid metabolism, and aging. Recently, honokiol (HKL), as apharmaceutical SIRT3 activator, has been observed to have a protective effect against pressureoverload-induced cardiac hypertrophy by increasing SIRT3 activity. In this study, we investigatedwhether HKL, as a SIRT3 activator, also has protective effects against unilateral ureteral obstruction(UUO)-induced renal tubulointerstitial fibrosis through SIRT3-dependent regulation ofmitochondrial dynamics and the nuclear factor-kappaB (NF-kappaB)/transforming growth factor-beta1 (TGF-beta1)/Smad signaling pathway. We found that HKL decreased the UUO-induced increase in tubularinjury and extracellular matrix (ECM) deposition in mice. HKL also decreased myofibroblastactivation and proliferation in UUO kidneys and NRK-49F cells. Finally, we showed that HKLtreatment decreased UUO-induced mitochondrial fission and promoted mitochondrial fusionthrough SIRT3-dependent effects. In conclusion, activation of SIRT3 via HKL treatment might havebeneficial effects on UUO-induced renal fibrosis through SIRT3-dependent regulation ofmitochondrial dynamics and the NF-kappaB/TGF-beta1/Smad signaling pathway.
- Journal
- Int J Mol Sci
- Publish Year
- 2020
- Experiment Subject
- mouse; nrk-49f cells
- Experiment Type
- Animal & Cell Experiment
- Phenotype Related
- Cardiac Hypertrophy; Chronic Kidney Diseases; Renal Fibrosis; Unilateral Ureteral Obstruction; Renal Tubulointerstitial Fibrosis
- Paper Title Cn
- Paper Title En
- Sirtuin 3 Activation by Honokiol Decreases Unilateral Ureteral Obstruction-Induced Renal Inflammation and Fibrosis via Regulation of Mitochondrial Dynamics and the Renal NF-κBTGF-β1/Smad Signaling Pathway
- Bilingual Status
- semi_complete