To navigate the mechanism of SP1 in sepsis, SP1 expression was silenced in LPS-treated H9C2 cardiomyocytes, and there showed relieved cardiomyocyte damage and inflammation, suppressed oxidative stress and apoptosis, and reduced HDAC4 and HIF-1α expression levels (Fig. 4A–N). This evidence concerns the gene HDAC4 and Sepsis.