2018
DOI: 10.1016/j.bbalip.2018.03.001
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Erythropoietin alleviates hepatic steatosis by activating SIRT1-mediated autophagy

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Cited by 25 publications
(28 citation statements)
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“…al. revealed a novel mechanism of alleviation of hepatic steatosis by EPO by activation of autophagy through SIRT1-dependent deacetylation of LC3 in the treatment of hepatic steatosis [38]. The data from the present study demonstrated that the anti-apoptotic effect following EPO pretreatment of BMSCs may be mediated though the SIRT1 pathway.…”
Section: Discussionsupporting
confidence: 53%
See 1 more Smart Citation
“…al. revealed a novel mechanism of alleviation of hepatic steatosis by EPO by activation of autophagy through SIRT1-dependent deacetylation of LC3 in the treatment of hepatic steatosis [38]. The data from the present study demonstrated that the anti-apoptotic effect following EPO pretreatment of BMSCs may be mediated though the SIRT1 pathway.…”
Section: Discussionsupporting
confidence: 53%
“…SIRT1 regulates a variety of cellular signaling pathways by modifying the acetylation status of target proteins, including p53, members of the forkhead family of transcription factors (FOXO), nuclear factor NF-κB, among others. Following activation, it participates in various cellular processes such as cell senescence, apoptosis, DNA damage repair, cell cycle, antioxidative stress, energy metabolism regulation, tumor generation, and other physiological and pathological processes [38][39][40]. P53 plays a vital role in the apoptotic signaling pathways, including membrane apoptotic signaling and mitochondrial apoptotic pathways, and affects the transcription and expression of many apoptosis-related cytokines in the nucleus [41].…”
Section: Discussionmentioning
confidence: 99%
“…EPO has been demonstrated to impede DOXinduced cardiotoxicity by activating SIRT1, leading to enhancement of mitochondrial function [20]. Hong et al revealed that EPO alleviates hepatic steatosis by activating autophagy through SIRT1dependent de-acetylation of LC3 [38]. In our study, most of the BMSCs undergo cell death after transplantation, mainly due to the adverse local microenvironment.…”
Section: Discussionsupporting
confidence: 48%
“…SIRT1 regulates a variety of cellular signaling pathways by modifying the acetylation status of target proteins including p53, members of the forkhead family of transcription factors (FOXO), and nuclear factor NF-κB. Following activation, SIRT1 participates in a plethora of cellular processes such as cell senescence, apoptosis, DNA damage repair, cell cycle, oxidative stress response, energy metabolism regulation, tumor generation, and other physiological and pathological processes [38][39][40]. Tumor suppressor protein, p53, plays a vital role in apoptotic signaling pathways, including membrane and mitochondrial apoptotic pathways, and affects the transcription and expression of many apoptosis-related cytokines in the nucleus [41].…”
Section: Discussionmentioning
confidence: 99%
“…EPO has been demonstrated to impede DOXinduced cardiotoxicity by activating SIRT1, leading to enhancement of mitochondrial function [18]. Hong et al revealed that EPO alleviates hepatic steatosis by activating autophagy through SIRT1dependent de-acetylation of LC3 [33]. SIRT1 plays an important role in maintaining the self-renewal and differentiation of MSCs, especially under stress conditions [39,40], and also exhibits positive effects on senescence and apoptosis of MSCs [41,42].…”
Section: Discussionmentioning
confidence: 99%