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Free fatty acid induced Nlrp3 inflammasome activation in mouse BMDMs

GSE267509 Mus musculus Expression profiling by high throughput sequencing 6 samples Submitted 2026/06/30 Platform GPL24247
Summary
In this manuscript, we focused on solving systemic inflammation in T2D. Chronic inflammation, is a well-established contributor to metabolic disorders such as type 2 diabetes (T2D). The Nlrp3 inflammasome appears substantial role in participating in the mechanism of T2D-induced inflammation. In the context of metabolic-inflammatory diseases like T2D, free fatty acid (FFAs) may serve as more pertinent activators of the Nlrp3 inflammasome compared to Nlrp3 regular activators like ATP. While limited works explored further mechanisms and therapy of Nlrp3 inflammasome dependent post–translational processing of proinflammatory cytokines in response to T2D-associated metabolic danger signals in the development of inflammatory-metabolic impairments.
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Also filed as BioProject PRJNA1111753 and SRA study SRP507751. Searching any of these in the dataset finder brings you back here.

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