Publications by authors named "Chuwei Yu"

Article Synopsis
  • SOS1 is a key guanine nucleotide exchange factor involved in RAS activation and is critical in leukemia development, but traditional inhibitors have had limited success in treating cancers related to KRAS and CML.
  • The study introduces a new compound, SIAIS562055, which effectively degrades SOS1 and inhibits the downstream ERK signaling pathway, showcasing stronger anti-cancer effects than existing small molecule inhibitors.
  • SIAIS562055 not only enhances the effectiveness of KRAS and BCR-ABL inhibitors but also shows promise in treating KRAS-mutant tumors and BCR-ABL+ chronic myeloid leukemia, suggesting that targeting SOS1 could be a valuable therapeutic strategy for these conditions.
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Epigenetic regulations play crucial roles in the pathogenesis of metabolic-associated fatty liver disease; therefore, elucidating the biological functions of differential miRNAs helps us to understand the pathogenesis. Herein, we discovered miR-337-3p was decreased in patients with NAFLD from Gene Expression Omnibus dataset, which was replicated in various cell and mouse models with lipid disorders. Subsequently, overexpression of miR-337-3p could ameliorate hepatic lipid accumulation, reduce fasting blood glucose, and improve insulin resistance.

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Non-alcoholic steatohepatitis (NASH) is a chronic liver disease characterized by hepatic steatosis, inflammation, and progressive fibrosis. Our previous study demonstrated that microRNA-552-3p (miR-552-3p) was down-regulated in the livers of patients with NASH and alleviated hepatic glycolipid metabolic disorders. However, whether miR-552-3p affects NASH progression remains unclear.

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Non-alcoholic fatty liver disease (NAFLD) is a chronic metabolic disease manifested in hepatic steatosis, inflammation, fibrosis, etc., which affects over one-quarter of the population around the world. Since no effective therapeutic drugs are available to cope with this widespread epidemic, the functional research of genes with altered expression during NAFLD helps understand the pathogenesis of this disease and the development of new potential therapeutic targets for drugs.

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Lipotoxicity induced by the overload of lipid in the liver, especially excess free cholesterol (FC), has been recognized as one of driving factors in the transition from non-alcoholic fatty liver (NAFL) to non-alcoholic steatohepatitis (NASH). MicroRNA (miR)-379-5p has been reported to play regulatory roles in hepatic triglyceride homeostasis, but the relationship of miR-379-5p and hepatic cholesterol homeostasis has never been touched. In the current study, we found that hepatic miR-379-5p levels were decreased obviously in NAFLD patients and model mice compared with their controls.

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Nonalcoholic fatty liver disease (NAFLD) is one of the most common metabolic diseases and closely associated with lipid disorder. Mitochondrion has been recognized to play a key role in lipid metabolism as the main site of energy metabolism in cells, and its dysfunction is involved in the progression of NAFLD. MicroRNAs (miRNAs), one of regulators in the pathogenesis of NAFLD, are discovered to modulate mitochondrial function by targeting mitochondrial proteins or mitochondrial-related factors, thereby improving or deteriorating NAFLD-associated pathologies.

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Background: Reducing serum low-density lipoprotein cholesterol (LDL-C) in hyperlipemia is recognized as an effective strategy to minimize the risk of atherosclerotic cardiovascular disease (ASCVD). MiR-337-3p has already been discovered to play regulatory roles in tumor proliferation and metastasis, adipocyte browning and ischemic brain injury, etc. However, the association between miR-337-3p and LDL-C is unknown.

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PCSK9 has emerged as a promising new therapeutic target for hyperlipidemia. The efficacy of PCSK9 siRNA in clinic trials clues the feasibility of exploring more PCSK9 inhibitors based on genetic inhibition in the treatment of hyperlipidemia. MicroRNAs (miRNAs) as a class of endogenous non-coding small RNAs can regulate genes at transcriptional and/or translational level.

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Background: Fostering self-directed learning skills in nursing students may provide a foundation for improving the specialty knowledge of these nurses.

Purpose: This study examines the current status of nursing student self-directed learning behavior and explores how different background factors impact self-directed learning.

Methods: This research design used a cross-sectional survey and convenience sampling.

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