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[The mechanism of GSK-3β/CREB signaling pathway regulating macrophage pyroptosis and participating in the occurrence and development of diabetic foot ulcer].
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi
December 2024
Department of Endocrinology, The Fourth Hospital of Changsha(Changsha Hospital of Hunan Normal University), Changsha 410000, China.
Objective To investigate the role and possible mechanism of glycogen synthase kinase-3 beta (GSK-3β)/cAMP response element binding protein (CREB) signaling pathway in regulating macrophage pyroptosis in the pathogenesis and development of diabetic foot ulcer (DFU). Methods Thirty rats were randomly divided into control group, DFU group and GSK-3β inhibited group, with 10 rats in each group. Fasting blood glucose (FBG) was detected by dynamic blood glucose detector.
View Article and Find Full Text PDFSerum HMGB-1 released by ferroptosis and necroptosis as a novel potential biomarker for systemic lupus erythematosus.
Int Immunopharmacol
October 2024
Department of Rheumatology and Clinical Immunology, The Second Affiliated Hospital of Kunming Medical University, Yunnan Province, Kunming 650101, China. Electronic address:
High mobility group box proterin-1 (HMGB-1) is a multifunctional protein that can be released by various programmed cell deaths (PCDs), such as necroptosis and ferroptosis. PCDs play a critical role in the pathogenesis of systemic lupus erythematosus (SLE). However, the role of HMGB-1 in the process of SLE remains unclear.
View Article and Find Full Text PDFHyperactivation of SREBP induces pannexin-1-dependent lytic cell death.
J Lipid Res
July 2024
Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Taikang Center for Life and Medical Sciences, Taikang Medical School, Wuhan University, Wuhan, China. Electronic address:
Sterol-regulatory element binding proteins (SREBPs) are a conserved transcription factor family governing lipid metabolism. When cellular cholesterol level is low, SREBP2 is transported from the endoplasmic reticulum to the Golgi apparatus where it undergoes proteolytic activation to generate a soluble N-terminal fragment, which drives the expression of lipid biosynthetic genes. Malfunctional SREBP activation is associated with various metabolic abnormalities.
View Article and Find Full Text PDFInterleukin-1-mediated hyperinflammation in XIAP deficiency is associated with defective autophagy.
Blood
September 2024
Cell Biology Program, SickKids Research Institute, Toronto, ON, Canada.
Deficiency of X-linked inhibitor of apoptosis protein (XIAP) is a rare genetic condition that can present with recurrent episodes of hemophagocytic lymphohistiocytosis (HLH), though the exact mechanisms leading to this hyperinflammatory disorder are unclear. Understanding its biology is critical to developing targeted therapies for this potentially fatal disease. Here, we report on a novel multiexonic intragenic duplication leading to XIAP deficiency with recurrent HLH that demonstrated complete response to interleukin (IL)-1β blockade.
View Article and Find Full Text PDFMice Hepatic Organoids for Modeling Nonalcoholic Fatty Liver Disease and Drug Response.
Stem Cells Dev
August 2024
Department of Hepatobiliary Pancreatic Surgery, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, China.
Article Synopsis
- * Researchers constructed NAFLD models using mouse liver organoids, observing significant changes such as lipid accumulation and increased liver enzymes after exposing them to free fatty acids (FFA).
- * The study identified alterations in key genes related to NAFLD and showed that compounds JC2-11 and lanifibranor reduced FFA-induced liver damage, indicating that these organoids are a useful tool for drug discovery in NAFLD.
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