Activation of Toll-Like Receptors and Inflammasome Complexes in the Diabetic Cardiomyopathy-Associated Inflammation

Figure 2

Crosstalk between TLRs, NLRP3 inflammasomes and dysregulated metabolic factors in DCM. PPARs and Sirt1 may control NLRP3 inflammasome and TLR pathways by interfering with the inflammasome assembly (1), proinflammatory gene overexpression (2), and NF-𝜅B signaling (3-4). In addition, Sirt1 could mediate PPARs activation by PGC1𝛼 deacetylation (5).