Curcumin, a polyphenolic compound derived from turmeric, has shown significant protective effects against cardiovascular diseases (CVDs). It protects cardiomyocytes from ischemia/reperfusion injury, inhibits myocardial hypertrophy and fibrosis, improves ventricular remodeling, reduces drug-induced myocardial injury, and alleviates vascular endothelial dysfunction. Curcumin also inhibits foam cell formation, reduces vascular smooth muscle cell (VSMC) proliferation, and improves diabetic cardiomyopathy (DCM). Clinical studies indicate that curcumin is safe, though high doses may cause liver damage and embryonic heart defects. Recent research highlights curcumin's mechanisms in CVDs, including its role in reducing oxidative stress via the Nrf2/HO-1 pathway, inhibiting inflammation through TLR4 and NF-κB pathways, and regulating lipid metabolism to prevent lipid plaque formation. Curcumin also promotes angiogenesis, protects VSMCs by inhibiting their migration and proliferation, and reduces vascular inflammation. In clinical trials, curcumin has been shown to improve endothelial function and vascular NO bioavailability. Additionally, curcumin inhibits cardiomyocyte apoptosis, hypertrophy, and fibrosis, and alleviates ventricular remodeling. It also plays a role in treating autoimmune myocarditis and DCM by reducing inflammation and promoting M2 macrophage polarization. Overall, curcumin's multifaceted mechanisms make it a promising therapeutic candidate for CVD prevention and treatment.Curcumin, a polyphenolic compound derived from turmeric, has shown significant protective effects against cardiovascular diseases (CVDs). It protects cardiomyocytes from ischemia/reperfusion injury, inhibits myocardial hypertrophy and fibrosis, improves ventricular remodeling, reduces drug-induced myocardial injury, and alleviates vascular endothelial dysfunction. Curcumin also inhibits foam cell formation, reduces vascular smooth muscle cell (VSMC) proliferation, and improves diabetic cardiomyopathy (DCM). Clinical studies indicate that curcumin is safe, though high doses may cause liver damage and embryonic heart defects. Recent research highlights curcumin's mechanisms in CVDs, including its role in reducing oxidative stress via the Nrf2/HO-1 pathway, inhibiting inflammation through TLR4 and NF-κB pathways, and regulating lipid metabolism to prevent lipid plaque formation. Curcumin also promotes angiogenesis, protects VSMCs by inhibiting their migration and proliferation, and reduces vascular inflammation. In clinical trials, curcumin has been shown to improve endothelial function and vascular NO bioavailability. Additionally, curcumin inhibits cardiomyocyte apoptosis, hypertrophy, and fibrosis, and alleviates ventricular remodeling. It also plays a role in treating autoimmune myocarditis and DCM by reducing inflammation and promoting M2 macrophage polarization. Overall, curcumin's multifaceted mechanisms make it a promising therapeutic candidate for CVD prevention and treatment.