IL1B and chronic kidney disease: TMAO plays an important role in the progression of CKD through the following mechanisms: TMAO exacerbates kidney injury by inducing oxidative stress [40,42]; TMAO is a potent pro-inflammatory factor, capable of activating the NLRP3 inflammasome and promoting the expression of inflammatory cytokines such as TNF-α, IL-6, and IL-1β [42,43,44]; TMAO further impairs kidney function by inducing endoplasmic reticulum stress; TMAO promotes kidney fibrosis by inducing ferroptosis in kidney tubular epithelial cells and the secretion of fibrotic factors [45,46].