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Atorvastatin Induces FXR and CYP7A1 Activation as a Result of the Sequential Action of PPAR γ/PGC-1α/HNF-4α in Hep3B Cells
CONCLUSIONS: Atorvastatin induces FXR and CYP7A1 activation as a result of sequential action of PPARγ-PGC-1α-HNF-4α in human hepatocytes. We propose that atorvastatin enhances solubility of cholesterol in bile by simultaneously activating of FXR and CYP7A1.PMID:33686046 | DOI:10.4166/kjg.2020.156
Source: Korean J Gastroenter... - March 9, 2021 Category: Gastroenterology Authors: Jin Lee Eun Mi Hong Jang Han Jung Se Woo Park Sang Pyo Lee Dong Hee Koh Hyun Joo Jang Sea Hyub Kae Source Type: research

Effect of atorvastatin on LOX-1 and eNOS expression in collateral vessels of hypercholesterolemic rats.
CONCLUSIONS: Both hypercholesterolemia and oxLDL can induce endothelial dysfunction and impair collateral vessel growth via the LOX-1/eNOS pathway in rats, and atorvastatin treatment can restore the LOX-1/eNOS pathway to promote the growth of the collateral vessels, suggesting the potential of atorvastatin as a therapeutic agent to promote repair of collateral vessel injuries in ischemic diseases. PMID: 31852645 [PubMed - in process]
Source: Journal of Southern Medical University - November 29, 2019 Category: Universities & Medical Training Authors: Yinjuan T, Jianjun W, Yinglu G, Weijun C, Weijun T, Mingying L Tags: Nan Fang Yi Ke Da Xue Xue Bao Source Type: research

Effect of atorvastatin on cardiomyocyte hypertrophy through suppressing MURC induced by volume overload and cyclic stretch.
Abstract MURC (muscle-restricted coiled-coil protein) is a hypertrophy-related gene. Hypertrophy can be induced by mechanical stress. The purpose of this research was to investigate the hypothesis that MURC mediates hypertrophy in cardiomyocytes under mechanical stress. We used the in vivo model of an aortocaval shunt (AV shunt) in adult Wistar rats to induce myocardial hypertrophy. We also used the in vitro model of cyclic stretch in rat neonatal cardiomyocytes to clarify MURC expression and the molecular regulation mechanism. The flexible membrane culture plate seeding with cardiomyocytes Cardiomyocytes seeded o...
Source: J Cell Mol Med - December 3, 2018 Category: Molecular Biology Authors: Cheng WP, Lo HM, Wang BW, Chua SK, Shyu KG Tags: J Cell Mol Med Source Type: research

Atorvastatin ameliorates LPS ‐induced inflammatory response by autophagy via AKT/mTOR signaling pathway
This article is protected by copyright. All rights reserved
Source: Journal of Cellular Biochemistry - August 3, 2017 Category: Biochemistry Authors: Fei Han, Qing ‐Qing Xiao, Shi Peng, Xin‐Yu Che, Li‐Sheng Jiang, Qin Shao, Ben He Tags: Article Source Type: research

Atorvastatin Alleviates Experimental Diabetic Cardiomyopathy by Regulating the GSK-3 β-PP2Ac-NF-κB Signaling Axis
by Xiao-min Ren, Guang-feng Zuo, Wen Wu, Jie Luo, Peng Ye, Shao-liang Chen, Zuo-ying Hu Recent studies reported that atorvastatin (ATOR) alleviated progression of experimental diabetic cardiomyopathy (DCM), possibly by protecting against apoptosis. However, the underlying mechanisms of this protective effect remain unclear. Therefore, our study investigated the role of the glycogen s ynthase kinase (GSK)-3β-protein phosphatase 2A(PP2A)-NF-κB signaling pathway in the anti-apoptotic and cardioprotective effects of ATOR on cardiomyocytes cultured in high glucose (HG) and in DCM. Our results showed that, in HG-cultured card...
Source: PLoS One - November 15, 2016 Category: Biomedical Science Authors: Xiao-min Ren Source Type: research

Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia
Conclusion Treatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia.
Source: Journal of the Formosan Medical Association - September 17, 2016 Category: Journals (General) Source Type: research

Atorvastatin alleviates cardiomyocyte apoptosis by suppressing TRB3 induced by acute myocardial infarction and hypoxia.
CONCLUSION: Treatment of atorvastatin inhibits the expression of TRB3 and cardiomyocyte apoptosis induced by AMI and hypoxia. PMID: 27645622 [PubMed - as supplied by publisher]
Source: J Formos Med Assoc - September 15, 2016 Category: Journals (General) Authors: Cheng WP, Lo HM, Wang BW, Chua SK, Lu MJ, Shyu KG Tags: J Formos Med Assoc Source Type: research

The anti ‑dengue virus properties of statins may be associated with alterations in the cellular antiviral profile expression.
The anti‑dengue virus properties of statins may be associated with alterations in the cellular antiviral profile expression. Mol Med Rep. 2016 Jul 13; Authors: Bryan-Marrugo OL, Arellanos-Soto D, Rojas-Martinez A, Barrera-Saldaña H, Ramos-Jimenez J, Vidaltamayo R, Rivas-Estilla AM Abstract Dengue virus (DENV) susceptibility to cholesterol depleting treatments has been previously reported. There are numerous questions regarding how DENV seizes cellular machinery and cholesterol to improve viral production and the effect of cholesterol sequestering agents on the cellular antiviral response. The aim of...
Source: Molecular Medicine Reports - July 21, 2016 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

Atorvastatin Inhibits Myocardial Apoptosis in a Swine Model of Coronary Microembolization by Regulating PTEN/PI3K/Akt Signaling Pathway
Conclusion: Modulation of PTEN was probably as a potential mechanism involved in the beneficial effects of pretreatment of atorvastatin to cardiac function and apoptosis in large animal models of CME.Cell Physiol Biochem 2016;38:207-219
Source: Cellular Physiology and Biochemistry - January 19, 2016 Category: Cytology Source Type: research

Statins up-regulate SmgGDS through {beta}1-integrin/Akt1 pathway in endothelial cells
Conclusion These results indicate that statins selectively up-regulate SmgGDS in endothelial cells, for which the β1-integrin/Akt1 pathway may be involved, demonstrating the novel aspects of the pleiotropic effects of statins.
Source: Cardiovascular Research - December 28, 2015 Category: Cardiology Authors: Minami, T., Satoh, K., Nogi, M., Kudo, S., Miyata, S., Tanaka, S.-i., Shimokawa, H. Tags: Vascular Biology Source Type: research

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