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Loss of glomerular aldolase B in diabetic nephropathy promotes renal fibrosis via activating Akt/GSK/β-catenin axis.

J Adv Res

December 2024

State Key Laboratory of Pharmaceutical Biotechnology, Department of Gastroenterology, Drum Tower Hospital, Nanjing University, School of Life Sciences, Nanjing, Jiangsu 210093, China. Electronic address:

Objective: Diabetic nephropathy (DN), characterized by a complex and multifaceted pathogenesis, stands as the foremost catalyst behind end-stage renal disease (ESRD). This study aims to analyze the level and non-metabolic role of glomerular aldolase B (ALDOB) in DN progression.

Methods: Glomerular proteomics and transcriptome are analyzed from 50 DN patients and 25 controls, respectively.

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Background/objective: Obesity and overweight have become growing health-related issues worldwide, which also applies to Poland. Excess fat mass is associated with an increased risk of metabolic and non-metabolic complications. The aim of our pre-post-designed study was to assess the effect of behavioral intervention on body weight, fat mass and anthropometric and metabolic parameters in obese and overweight individuals.

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Neuroinflammation is a prominent feature of Alzheimer's disease (AD). Activated microglia undergo a reprogramming of cellular metabolism necessary to power their cellular activities during disease. Thus, selective targeting of microglial immunometabolism might be of therapeutic benefit for treating AD.

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The ketogenic diet (KD) is recognized as minimum carbohydrate and maximum fat intakes, which leads to ketosis stimulation, a state that is thought to metabolize fat more than carbohydrates for energy supply. KD has gained more interest in recent years and is for many purposes, including weight loss and managing serious diseases like type 2 diabetes. On the other hand, many believe that KD has safety issues and are uncertain about the health drawbacks.

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Search progress of pyruvate kinase M2 (PKM2) in organ fibrosis.

Mol Biol Rep

March 2024

Department of Cardiology, Hospital of Jiangsu University, Zhenjiang, Jiangsu, 212000, China.

Fibrosis is characterized by abnormal deposition of the extracellular matrix (ECM), leading to organ structural remodeling and loss of function. The principal cellular effector in fibrosis is activated myofibroblasts, which serve as the main source of matrix proteins. Metabolic reprogramming, transitioning from mitochondrial oxidative phosphorylation to aerobic glycolysis, is widely observed in rapidly dividing cells such as tumor cells and activated myofibroblasts and is increasingly recognized as a fundamental pathogenic basis in organ fibrosis.

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