Previous studies have shown that dapagliflozin can reduce the myocardial oxidative stress and inhibit the expression of inflammatory factors like TNF-α, IL-1β, IL-6, and MCP-1 in myocardium by the reduction of malonaldehyde and the increase of superoxide dismutase, thus inhibiting the myocardial hypertrophy and myocardial fibrosis [23–25]. Here, CCL2 is linked to Myocardial fibrosis.