Mechanistic investigations further integrated molecular docking, immunoprecipitation (IP), microscale thermophoresis (MST), surface plasmon resonance (SPR), and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to define the molecular targets and JAK1/STAT1 signaling pathways underlying CVB-D activity.<h4>Results</h4>CVB-D treatment robustly improved mitochondrial dysfunction in Diabetic cardiomyopathy and attenuated heart failure-like phenotypes in cardiomyocytes both in vivo and in vitro. The gene discussed is JAK1; the disease is diabetic cardiomyopathy.