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AMPK mTOR Autophagy - Crossref

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Last Updated: 02 May 2022

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Long Non-Coding LEF1-AS1 Sponge miR-5100 Regulates Apoptosis and Autophagy in Gastric Cancer Cells via the miR-5100/DEK/AMPK-mTOR Axis

The role of miR-5100 and DEK's autophagy and apoptosis in gastric cancer is still unclear, as well as the role between miR-5100 and DEK's regulatory system. DEK was highly present in gastric cancer tissues and cell lines, and knockdown of DEK stifled cell autophagy, promoted apoptosis, and minimized the malignant phenotype of gastric cancer. MiR-5100 is used by miR-5100 in attacking the 3′UTR of DEK, according to studies, and LEF1-AS1 controls miR-5100's expression by sponging with mIR-5100.

Source link: https://doi.org/10.3390/ijms23094787


Luteolin ameliorated CHC-induced autophagy dysfunction in macrophages through the AMPK/mTOR signaling pathway

Aim This experiment is designed to see if Lut can correct macrophage dysfunction caused by CHC, whether it reduces macrophages caused by CHC, and whether it can minimize macrophages caused by CHC's apoptosis. Methods The RAW264. 7 macrophages were modeled with CHC, and the correct amount of Lut was used to start treating the inflammatory model macrophages. Until now, the effect of Lut on the autophagy pathway AMPK and mTOR in inflammation modeling with CHC was investigated. The following reactions are contradictory after Lut intervenes in macrophages following CHC's steps. Lut can cause autophagy dysfunction caused by CHC and reduce apoptosis caused by macrophagy inhibition that has been reduced by macrophage autophagy. Lut can control the apoptosis of macrophages caused by CHC through the AMPK/mTOR signaling pathway.

Source link: https://doi.org/10.21203/rs.3.rs-1580418/v1


hUMSC transplantation restores ovarian function in POI rats by inhibiting autophagy of theca-interstitial cells via the AMPK/mTOR signaling pathway

Abstract Bibliography Previous studies of primary ovarian insufficiency have concentrated on granulosa cells and ignored the role of theca-interstitial cells. This study intends to investigate the mechanisms of human umbilical cord-derived mesenchymal stem cell proliferation in POI rats by limiting autophagy of TICs. By tail vein, the hUMSCs were transplanted into POI rats. POI rats' infected with TICs in vivo and hUMSC transplantation improved the ovarian function and reduced the apoptosis of TICs. Conclusion This research shows that hUMSCs protected ovarian function in POI by regulating autophagy signaling pathway AMPK/mTOR.

Source link: https://doi.org/10.1186/s13287-020-01784-7


Quercetin activates autophagy suppresses apoptosis, inflammation and cartilage matrix degradation in LPS-induced chondrocytes through targeting AMPK/mTOR/ULK1 signaling pathway

Abstract Background: Osteoarthritis is a chronic joint disease characterized by degeneration of articular cartilage, a mass apoptosis of chondrocytes, and changes in subchondral bone. We examined the protective effects of QUE on restoring OA-induced chondrocyte injury and its potential mechanisms in this report. The Com C+QUE+LPS induction group and the Com C+QUE+LPS induction group were divided into Control group, LPS induction group, 3-MA+LPS induction group, 3-MA+LPS induction group, 3-MA+LPS induction group, Com C+QUE+LPS induction group, Com C+QUE+LPS induction group, Com C+QUE+LPS induction group, and Com C+QUE+LPS induction group, The Cell Cycle Kit 8 assay, osteoarthritis, and inflammatory factors relevant to osteoarthritis, interleukin1 and tumor necrosis factor were determined by enzyme-linked immunosorbent assay. Result: In the current study, we found that QUE can induce autophagy in LPS-induced chondrocytes. These findings also showed that QUE activates autophagy can inhibit apoptosis, inflammation, and cartilage matrix degradation in LPS-induced chondrocytes by targeting the AMPK/ULK1 signaling pathway.

Source link: https://doi.org/10.21203/rs.3.rs-1541634/v1


PLCL1 suppresses tumor progression by regulating AMPK/mTOR-mediated autophagy in renal cell carcinoma

phospholipase C-like protein 1 is found in lipid metabolism of clear cell renal cell carcinomas, according to a previous study. Result: Bioinformatics analysis showed and confirmed that the expression of PLCL1 is reduced in tumors and is closely linked to prognosis in ccRCC patients. Elevated PLCL1 levels decreased proliferation capacity and invasion when promoting apoptosis, but the PLCL1 knockdown reversed these changes in ccRCC cells compared to controls. The results in mouse models showed that PLCL1 reduces ccRCC tumor formation. PLCL1 may be a promising target for the treatment of ccRCC patients.

Source link: https://doi.org/10.21203/rs.3.rs-1501645/v1


Emodin Ameliorate High Glucose-induced Podocyte Apoptosis via Regulating AMPK/mTOR- mediated Autophagy Signaling Pathway

Abstract Background: Podocyte apoptosis and autophagy dysfunction have been cited as two of diabetic nephropathy's most common causes of diabetic nephropathy. In vitro, the present research was done to determine the effect of emodin on elevated glucose-induced podocyte apoptosis and whether the possible anti-inflammatory mechanism of emodin is related to the induction of AMPK/mTOR-mediated autophagy in MPC5 cells. The expression of Cleaved caspase-3, autophagy manufacturer LC3 I/II, and AMPK/mTOR signaling pathway-related proteins were determined by western blot analysis. Results: HG dose-dependently induced cell apoptosis in MPC5 cells, but emodin significantly improved HG-induced cell death and caspase-3 cleavage. In MPC5 cells, Emodin significantly raised LC3-III levels and promoted RFP-LC3-containing punctate structures. The AMPK inhibitor compound C, which was omitted from emodin-mediated autophagy activation, has been shut down. In vitro, emodin ameliorated HG-induced autophagy in MPC5 cells, resulting in autophagy development via the AMPK/mTOR signaling pathway, which may be a potential therapeutic option for DN.

Source link: https://doi.org/10.21203/rs.3.rs-796405/v1


Graphene oxide induces autophagy and apoptosis via ROS-dependent AMPK/mTOR/ULK-1 pathway in colorectal cancer cells

Aim: To investigate the anticancer effects and action mechanism of graphene oxide in colorectal cancer. Both in vivo and in vitro, materials and methods: Anticancer effects and mechanisms of GO in CRC were investigated both in vivo and in vitro. GO significantly reduced tumor formation both in vitro and in vivo. GO was able to enter HCT116 cells by endocytosis.

Source link: https://doi.org/10.2217/nnm-2022-0030


Taurine, EGCG and Genistein regulate AMPK-mTOR pathway to inhibit hepatic stellate cells autophagy and alleviate liver fibrosis in rats

Abstract Embedition of hepatic stellate cells is the most important factor in fibrosis progression in hepatic fibrosis. TEG reduced the expression of autophagy marker proteins LC3-III and Beclin1 in HSCs or fibrotic rats, according to western blot and IHC results. After TEG-treated HSCs, green fluorescence increased after TEG treatment HSCs, according to mRFP-GFP-LC3. TEG inhibitors inhibited LC3, Beclin1, AMPK, and mTOR genes, as well as phosphorylated protein expression in HSCs, according to a AMPK-mTOR pathway review. Our findings indicate that TEG anti-fibrotic can reduce autophagosomes by blocking the AMPK-mTOR pathway.

Source link: https://doi.org/10.21203/rs.3.rs-1504132/v1


Decorin Protects Retinal Pigment Epithelium Cells from Oxidative Stress and Apoptosis via AMPK-mTOR-Regulated Autophagy

Although DCN has been shown to play a cytoprotective role in a variety of cell types, its protective properties against H2O2-induced oxidative stress and apoptosis in ARPE-19 cells are uncertain. In this research, we found that DCN significantly reduced cell viability loss, apoptosis rate, and reactive oxygen species levels in ARPE-19 cells induced by H2O2. These findings, taken together, show that DCN may be able to shield RPE cells from H2O2-induced oxidative stress and autophagy promotion, thus giving AMD prevention and therapy the therapeutic option for AMD prevention and treatment.

Source link: https://doi.org/10.1155/2022/3955748


Abstract 032: Impaired Cardiac Autophagy In Metabolic Syndrome Despite Intact AMPK And mTOR Signaling

After ischemic preconditioning, we previously reported that basal cardiac autophagy is lower in the setting of metabolic syndrome and is associated with attenuation of cardioprotection. Adult rat ventricular cardiomyocytes isolated from Sprague Dawley and Zucker obese rats showed how to analyze the underlying mechanisms and exclude effects of the extracellular environment. We investigated the roles of two key cellular energy sensing pathways, adenosine monophosphate-activated protein kinase and mammalian victim of rapamycin in order to determine the role of two key cellular energy sensing pathways, adenosine monophosphate In ARVM from SD rats, starvation, or Ph, increased p-AMPK and decreased p-70S6K, along with an elevated LC3-IIII and 50% reduction in p62. Rapamycin reduced phosphorylation of p70S6K, raised LC3-III, and decreased p62. In ZO ARVM, Ph and Rap also activated AMPK and halted mTOR; however, LC3-III was unchanged, and p62 clearance was reduced. Autophagy is impaired in ARVM from ZO rats despite correct activation of AMPK and inhibition of mTOR.

Source link: https://doi.org/10.1161/res.113.suppl_1.a032

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* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions