Coronary heart disease (CHD) is a chronic cardiovascular disease with coronary atherosclerosis as the main pathological basis. Its occurrence and progression are not a simple process of lipid deposition, but a systemic pathological process jointly driven by metabolic disorders, chronic low-grade inflammation, and immune imbalance. Recent studies have shown that endothelial dysfunction is a key event in the early occurrence of CHD. Abnormal lipid metabolism, immune cell infiltration, and continuous activation of inflammatory signals together promote plaque formation, maturation, and destabilization. Especially under the regulation of the metabolism-inflammation-immunity network, a positive feedback loop is formed between immune cell metabolic reprogramming, macrophage polarization, inflammasome activation, and oxidative stress response, which accelerates the progression of atherosclerosis and increases the risk of acute coronary events. Traditional therapeutic strategies centered on lipid-lowering, antiplatelet therapy, and revascularization can reduce the incidence of short-term events, but there are still limitations in long-term risk control and fundamental reversal of the disease.
Coronary heart disease (CHD) is a chronic cardiovascular disease with coronary atherosclerosis as the main pathological basis. Its occurrence and progression are not a simple process of lipid deposition, but a systemic pathological process jointly driven by metabolic disorders, chronic low-grade inflammation, and immune imbalance. Recent studies have shown that endothelial dysfunction is a key event in the early occurrence of CHD. Abnormal lipid metabolism, immune cell infiltration, and continuous activation of inflammatory signals together promote plaque formation, maturation, and destabilization. Especially under the regulation of the metabolism-inflammation-immunity network, a positive feedback loop is formed between immune cell metabolic reprogramming, macrophage polarization, inflammasome activation, and oxidative stress response, which accelerates the progression of atherosclerosis and increases the risk of acute coronary events. Traditional therapeutic strategies centered on lipid-lowering, antiplatelet therapy, and revascularization can reduce the incidence of short-term events, but there are still limitations in long-term risk control and fundamental reversal of the disease. From a narrative perspective, this article summarizes the research progress of CHD in pathological mechanisms, metabolism and immune regulation, plaque instability, and risk factors from a systematic perspective and focuses on discussing the potential value of multilevel and systematic intervention strategies in the precise prevention and treatment of CHD, providing a theoretical basis for future translational research and personalized treatment.