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Fig. 1 | Inflammation and Regeneration

Fig. 1

From: Molecular mechanism of crosstalk between immune and metabolic systems in metabolic syndrome

Fig. 1

Potential mechanism of metabolic and epigenetic regulation of TLR4 signaling. ER is an interface between immune and metabolic systems. PERK and IRE1α, along with their downstream effectors, ATF4 and XBP1, respectively, are involved in SFA-induced metabolic inflammatory responses. TLR4 signal–mediated proinflammatory cytokines are divided into the following two groups. Primary response genes are rapidly upregulated in response to stimuli, while secondary response genes are induced later. Accumulating evidence has highlighted the significant role of chromatin remodeling in the regulation of these upon TLR4 activation. Among others, covalent modifications at histones H3 and H4 have been shown to play a key role in regulating chromatin assembly and the recruitment of inducible transcription factors, suggesting the epigenetic regulation of TLR4 signaling. Created with BioRender.com

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