Figure 2.

Examining SCFAs in combating NF-κB-associated inflammation and cancer risk is crucial due to the complexity of inflammatory pathways in carcinogenesis. NF-κB up-regulates matrix metalloproteinases (MMPs), aiding metastasis, enhances VEGF for angiogenesis, and affects STAT signaling for cell proliferation while inhibiting apoptosis—key cancer progression traits. SCFAs counteract these by promoting T-cell differentiation into regulatory cells, stimulating anti-inflammatory cytokines, and upregulating tissue inhibitors of metalloproteinases (TIMPs) to reduce metastasis and block NF-κB and STAT pathways. Activation of NF-κB and the NLRP3 inflammasome is essential but concerning for TMAO-induced vascular calcification. The NLRP3 inflammasome’s role in inflammation complicates understanding chronic inflammation’s impact on blood vessels. This figure was created with BioRender software version 04.