At the level of inflammatory mechanisms, the chronic low-grade inflammatory state unique to diabetes continuously activates monocytes and macrophages through the NF-κB pathway, releasing pro-inflammatory factors such as TNF-α and IL-6, which not only directly damage the integrity of cardiomyocyte membranes but also trigger oxidative stress via the up-regulation of inducible nitric oxide synthase, leading to dysfunction of sarcoplasmic reticulum calcium-ion regulatory proteins. Here, NFKB1 is linked to diabetes mellitus.