Nagoya University · Medicine
Professor Noriko Satoh-Asahara's research lab focuses on the molecular mechanisms linking metabolic disorders—such as obesity, type 2 diabetes, and nonalcoholic steatohepatitis (NASH)—to systemic complications including cardiovascular disease, renal dysfunction, and neurodegeneration. Her team investigates the roles of bioactive molecules like EPA, U-CysC, myokines (e.g., CXCL1), and natural compounds (e.g., taxifolin) in modulating inflammation, oxidative stress, and tissue homeostasis. The lab integrates preclinical models with translational biomarker discovery to identify novel therapeutic targets and risk indicators for metabolic and age-related diseases.
Figures are computed from collected data and may differ slightly.
This study is the first to show that EPA increases the monocyte IL-10 expression in parallel with decrease of arterial stiffness, which may contribute to the antiatherogenic effect of EPA in obese dyslipidemic patients.
This study demonstrates that UCCR is significantly associated with renal dysfunction, the severity of MS, arterial stiffness, and weight change in obese patients. The data of this study suggest that U-CysC could serve as a CVD and CKD risk factor in patients with obesity and MS.
Dapagliflozin add-on therapy in patients with type 2 diabetes reduced myostatin levels significantly and maintained SMM, without significant changes in FGF21 levels.
Type 2 diabetes mellitus is associated with an increased risk of dementia, potentially through multifactorial pathologies, including neuroinflammation. Therefore, there is a need to identify novel agents that can suppress neuroinflammation and prevent cognitive impairment in diabetes. In the present study, we demonstrated that a high-glucose (HG) environment elevates the intracellular reactive oxygen species (ROS) levels and triggers inflammatory responses in the mouse microglial cell line BV-2.
The molecular pathogenesis of nonalcoholic steatohepatitis (NASH) includes a complex interaction of metabolic stress and inflammatory stimuli. Considering the therapeutic goals of NASH, it is important to determine whether the treatment can prevent the progression from NASH to hepatocellular carcinoma. Taxifolin, also known as dihydroquercetin, is a natural bioactive flavonoid with antioxidant and anti-inflammatory properties commonly found in various foods and health supplement products. In thi
These results suggest that secretion of the myokine CXCL1 is stimulated by saturated fatty acids and that CXCL1 promotes myogenesis from satellite cells to maintain skeletal muscle homeostasis.
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