<i>Retracted</i>: Sirt3 activation attenuated oxidized low‐density lipoprotein‐induced human umbilical vein endothelial cells’ apoptosis by sustaining autophagy by Luo, X, Yang, Z, Zheng, S, Cao, Y and Wu, Y

Luo, Xian-Du; Yang, Zhiqiang; Zheng, Shuai; Cao, Yong

doi:10.1002/cbin.10291

Cited by 12 publications

(6 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results that knockdown of Sirt3 expression partially prevented the autophagy and protection induced by resveratrol, further supported the involvement of Sirt3 in autophagy regulation in neuronal cells, and indicated that resveratrol-induced protective effects were mediated by Sirt3 signaling. However, the role of Sirt3 in autophagy regulation has not been fully determined, especially some results was shown to be irreproducible ( 2017 ), and thus, some more experiments in gene knockout animals need to be performed in the future.…”

Section: Discussionmentioning

confidence: 99%

Sirt3-Mediated Autophagy Contributes to Resveratrol-Induced Protection against ER Stress in HT22 Cells

et al. 2018

View full text Add to dashboard Cite

Endoplasmic reticulum (ER) stress occurring in stringent conditions is critically involved in neuronal survival and death. Resveratrol is a non-flavonoid polyphenol that has neuroprotective effects against many neurological disorders. Here, we investigated the potential protective effects of resveratrol in an in vitro ER stress model mimicked by tunicamycin (TM) treatment in neuronal HT22 cells. We found that TM dose-dependently decreased cell viability and increased apoptosis, which were both significantly attenuated by resveratrol treatment. Resveratrol markedly reduced the expression or activation of ER stress-associated factors, including GRP78, CHOP, and caspase-12. The results of immunocytochemistry and western blot showed that resveratrol promoted autophagy in TM-treated cells, as evidenced by increased LC3II puncta number, bcelin1 expression and LC3II/LC3I ratio. Pretreatment with the autophagy inhibitor chloroquine could reduce the protective effects of resveratrol. In addition, the expression of Sirt3 protein and its downstream enzyme activities were significantly increased in resveratrol-treated HT22 cells. To confirm the involvement of Sirt3-mediated mechanisms, siRNA transfection was used to knockdown Sirt3 expression in vitro. The results showed that downregulation of Sirt3 could partially prevented the autophagy and protection induced by resveratrol after TM treatment. Our study demonstrates a pivotal role of Sirt3-mediated autophagy in mediating resveratrol-induced protection against ER stress in vitro, and suggests the therapeutic values of resveratrol in ER stress-associated neuronal injury conditions.

show abstract

Section: Discussionmentioning

confidence: 99%

Sirt3-Mediated Autophagy Contributes to Resveratrol-Induced Protection against ER Stress in HT22 Cells

et al. 2018

View full text Add to dashboard Cite

show abstract

“…Previous studies have found that downregulation of SIRT3 promotes the apoptosis of alveolar epithelial cells ( 26 ) and EC9706 cells ( 27 ). Studies have also shown that SIRT3 protects tumor cells against apoptosis under unfavorable environments, such as hypoxia ( 28 ), oxidized low-density lipoprotein ( 29 ) and high glucose levels ( 30 ). However, the expression of SIRT3 and its effect on apoptosis and bronchial inflammation in asthma remains to be elucidated.…”

Section: Introductionmentioning

confidence: 99%

SIRT3 regulates bronchial epithelium apoptosis and aggravates airway inflammation in asthma

Song

Wang

2022

Mol Med Rep

View full text Add to dashboard Cite

Sirtuin (SIRT)3 is closely related to inflammation and apoptosis and studies have described this relationship, including in the lungs. However, the expression of SirT3 and its effect on apoptosis and inflammation in bronchial tissue in asthma remains to be elucidated. The present study found that SirT3 expression decreased in the bronchial tissues of asthmatic mice and its upregulation could not only reduce increased bronchial epithelial cells apoptosis in the asthmatic mice but also significantly decreased the elevated expression of cytokines (TnF-α, il-4, il-5 and il-13) in bronchoalveolar lavage fluid. Further study found that SIRT3 overexpression significantly decreased apoptosis-related protein expression (Bax/Bcl2 ratio and caspase 3 activity) and oxidative injury. In vitro, SirT3 regulated oxidative stress-induced bronchial epithelial cell (16HBe) apoptosis and cytokine expression. in conclusion, SirT3 expression decreased in bronchial tissues of asthmatic mice and the upregulation of SIRT3 expression could reduce the apoptosis of bronchial epithelium and airway inflammation. It was concluded that SIRT3 might be a potential target in asthma treatment.

show abstract

“…a key enzyme in the metabolic regulation and ROS homeo-435 stasis during vascular disease[95][96][97] (Fig. 2).…”

mentioning

confidence: 99%

Sirtuins in vascular diseases: Emerging roles and therapeutic potential

D’Onofrio

Vitiello

Casale

et al. 2015

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

View full text Add to dashboard Cite

Silent information regulator-2 (Sir-2) proteins, or sirtuins, are a highly conserved protein family of histone deacetylases that promote longevity by mediating many of the beneficial effects of calorie restriction which extends life span and reduces the incidence of cancer, cardiovascular disease (CVD), and diabetes. Here, we review the role of sirtuins (SIRT1-7) in vascular homeostasis and diseases by providing an update on the latest knowledge about their roles in endothelial damage and vascular repair mechanisms. Among all sirtuins, in the light of the numerous functions reported on SIRT1 in the vascular system, herein we discuss its roles not only in the control of endothelial cells (EC) functionality but also in other cell types beyond EC, including endothelial progenitor cells (EPC), smooth muscle cells (SMC), and immune cells. Furthermore, we also provide an update on the growing field of compounds under clinical evaluation for the modulation of SIRT1 which, at the state of the art, represents the most promising target for the development of novel drugs against CVD, especially when concomitant with type 2 diabetes.

show abstract

Retracted: Sirt3 activation attenuated oxidized low‐density lipoprotein‐induced human umbilical vein endothelial cells’ apoptosis by sustaining autophagy by Luo, X, Yang, Z, Zheng, S, Cao, Y and Wu, Y

Cited by 12 publications

References 0 publications

Sirt3-Mediated Autophagy Contributes to Resveratrol-Induced Protection against ER Stress in HT22 Cells

Sirt3-Mediated Autophagy Contributes to Resveratrol-Induced Protection against ER Stress in HT22 Cells

SIRT3 regulates bronchial epithelium apoptosis and aggravates airway inflammation in asthma

Sirtuins in vascular diseases: Emerging roles and therapeutic potential

Contact Info

Product

Resources

About