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Mon. Mar 17, 2025

Tue. Mar 18, 2025

Wed. Mar 19, 2025

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Fibroblast-specific PRMT5 deficiency and pharmacological PRMT5 inhibiton suppress cardiac fibrosis and left ventricular dysfunction in mice

Th17, which contributes to the worsening of autoimmune diseases (eg. Multiple sclerosis, Periodontal disease), enhances glucose metabolism. Tregs, which contributes to the suppression of autoimmune diseases, enhances lipid metabolism. On the other hand, aging contributes to a decline in glucose metabolism, pathogenicity of Th17 and is also considered a risk factor for autoimmune diseases.Periodontal disease, which increases with age, is related to the crosstalk between the microbiome, bone resorption, and Th17, and findings on this crosstalk were presented from the perspective of metabolism. Periodontal disease is also a risk factor for heart failure. It is known that cardiac fibrosis occurs with the progression of heart failure, and metabolism is also involved in the control mechanism.In this session, we will introduce findings that elucidate inflammation and disease from a metabolic perspective, and hope to promote interdisciplinary research between anatomy and pharmacology. We also expect that discuss about metabolism as a new therapeutic target.

Inflammation, disease and metabolism

APPW2025

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[[OD]2S13a-2]Fibroblast-specific PRMT5 deficiency and pharmacological PRMT5 inhibiton suppress cardiac fibrosis and left ventricular dysfunction in mice

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