Recent studies have indicated that the primary mechanisms by which TLR4/NF-kB exacerbates myocardial infarction encompass inflammation [123], oxidative stress [124], and pyroptosis—an inflammatory form of cell death that governs cardiomyocyte loss post-myocardial infarction—as well as apoptosis [125,126]. Here, TLR4 is linked to myocardial infarction.