The kynurenine pathway (KP) is the primary route for tryptophan metabolism in most mammals, with its downstream metabolites playing key roles in physiological and pathological processes. Indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) are the initial enzymes of the KP, with IDO playing a critical role in cardiovascular diseases. Elevated levels of kynurenine (KYN) and its metabolites have been observed in various cardiovascular diseases, such as atherosclerosis, hypertension, and acute myocardial infarction. KYN and its metabolites have complex roles in inflammation, exhibiting both inhibitory and stimulatory effects under different conditions. In atherosclerosis, IDO upregulation stimulates KYN production, mediating vascular inflammation and foam cell formation. In arterial calcification, this process alleviates osteogenic differentiation of vascular smooth muscle cells. In cardiac remodeling, KYN-mediated AhR activation exacerbates pathological left ventricular hypertrophy and fibrosis. Targeting KP components, such as IDO inhibitors, 3-hydroxyanthranilic acid, and anthranilic acid, demonstrates cardiovascular protective effects. This review outlines the mechanistic roles of KP in coronary atherosclerosis, arterial calcification, and myocardial diseases, highlighting its potential diagnostic, prognostic, and therapeutic value in cardiovascular diseases. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation.The kynurenine pathway (KP) is the primary route for tryptophan metabolism in most mammals, with its downstream metabolites playing key roles in physiological and pathological processes. Indoleamine 2,3-dioxygenase (IDO) and tryptophan 2,3-dioxygenase (TDO) are the initial enzymes of the KP, with IDO playing a critical role in cardiovascular diseases. Elevated levels of kynurenine (KYN) and its metabolites have been observed in various cardiovascular diseases, such as atherosclerosis, hypertension, and acute myocardial infarction. KYN and its metabolites have complex roles in inflammation, exhibiting both inhibitory and stimulatory effects under different conditions. In atherosclerosis, IDO upregulation stimulates KYN production, mediating vascular inflammation and foam cell formation. In arterial calcification, this process alleviates osteogenic differentiation of vascular smooth muscle cells. In cardiac remodeling, KYN-mediated AhR activation exacerbates pathological left ventricular hypertrophy and fibrosis. Targeting KP components, such as IDO inhibitors, 3-hydroxyanthranilic acid, and anthranilic acid, demonstrates cardiovascular protective effects. This review outlines the mechanistic roles of KP in coronary atherosclerosis, arterial calcification, and myocardial diseases, highlighting its potential diagnostic, prognostic, and therapeutic value in cardiovascular diseases. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation. The KP is involved in various cardiovascular diseases, including inflammation, atherosclerosis, arterial calcification, and myocardial diseases. The KP's role in cardiovascular diseases is complex, with both pathogenic and compensatory mechanisms. The KP is a double-edged sword in chronic inflammatory diseases. The KP's involvement in cardiovascular diseases is a subject of debate. The KP's role in atherosclerosis may vary depending on cell types. The KP may have diverse effects on disease progression concerning immunity and inflammation.