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| http://dx.doi.org/10.1113/jphysiol.1916.sp001746 | DOI Listing |
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Metabolic adaptations to acute glucose uptake inhibition converge upon mitochondrial respiration for leukemia cell survival.
Cell Commun Signal
January 2025
Department of Oncological Sciences, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY, 10029, USA.
One hallmark of cancer is the upregulation and dependency on glucose metabolism to fuel macromolecule biosynthesis and rapid proliferation. Despite significant pre-clinical effort to exploit this pathway, additional mechanistic insights are necessary to prioritize the diversity of metabolic adaptations upon acute loss of glucose metabolism. Here, we investigated a potent small molecule inhibitor to Class I glucose transporters, KL-11743, using glycolytic leukemia cell lines and patient-based model systems.
View Article and Find Full Text PDFThe PKM2 activator TEPP-46 suppresses cellular senescence in hydrogen peroxide-induced proximal tubular cells and kidney fibrosis in CD-1 mice.
J Diabetes Investig
January 2025
Faculty of Medicine, Internal Medicine, Shimane University, Izumo, Shimane, Japan.
Aim/introduction: Senescence is a key driver of age-related kidney dysfunction, including diabetic kidney disease. Oxidative stress activates cellular senescence, induces abnormal glycolysis, and is associated with pyruvate kinase muscle isoform 2 (PKM2) dysfunction; however, the mechanisms linking PK activation to cellular senescence have not been elucidated. We hypothesized that PKM2 activation by TEPP-46 could suppress oxidative stress-induced renal tubular cell injury and cellular senescence.
View Article and Find Full Text PDFUncovering glycolysis-driven molecular subtypes in diabetic nephropathy: a WGCNA and machine learning approach for diagnostic precision.
Biol Direct
January 2025
Department of Urology, The First Affiliated Hospital of Guangxi Medical University, Nanning, 530021, Guangxi, China.
Introduction: Diabetic nephropathy (DN) is a common diabetes-related complication with unclear underlying pathological mechanisms. Although recent studies have linked glycolysis to various pathological states, its role in DN remains largely underexplored.
Methods: In this study, the expression patterns of glycolysis-related genes (GRGs) were first analyzed using the GSE30122, GSE30528, and GSE96804 datasets, followed by an evaluation of the immune landscape in DN.
m6A demethylase Fto inhibited macrophage activation and glycolysis in diabetic nephropathy via m6A/Npas2/Hif-1α axis.
FASEB J
January 2025
Department of Nephropathy, The First Affiliated Hospital of Anhui Medical University, Anhui Medical University, Hefei, Anhui, People's Republic of China.
Macrophage infiltration and activation is a key factor in the progression of diabetic nephropathy (DN). However, aerobic glycolysis induced by m6A methylation modification plays a key role in M1-type activation of macrophages, but the specific mechanism remains unclear in DN. In this study, the expression of m6A demethylase Fto in bone marrow derived macrophages and primary kidney macrophages from db/db mice.
View Article and Find Full Text PDFIntroduction: Advanced glycation end products (AGEs) play a critical role in the development of vascular diseases in diabetes. Although stem cell therapies often involve exposure to AGEs, the impact of this environment on extracellular vesicles (EVs) and endothelial cell metabolism remains unclear.
Methods: Human umbilical cord mesenchymal stem cells (MSCs) were treated with either 0 ng/ml or 100 ng/ml AGEs in a serum-free medium for 48 hours, after which MSC-EVs were isolated.
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