Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
Cardiovascular Diseases
Cardiovascular disease refers to a group of diseases involving the heart and vascular system, including coronary heart disease, hypertension, myocardial infarction, stroke, etc. These diseases often involve structural and functional abnormalities of the cardiovascular system, which may lead to insufficient blood supply, heart dysfunction, and more. Risk factors for cardiovascular disease include high blood pressure, high cholesterol, diabetes, smoking, poor diet and lack of exercise. Preventive measures include maintaining a healthy lifestyle, regular physical examinations, and timely treatment of chronic diseases, which can help reduce the risk of cardiovascular disease.
Related Experimental Schemes
