Table 7 In vitro models of acquired cardiac diseases
Disease | Modeling strategy | Features | In vitro models | Ref. |
|---|---|---|---|---|
Myocardial Infarction | Cryoinjury | Fibronectin and collagen accumulation Necrosis Limited cardiomyocyte proliferation | CO | |
Oxygen-diffusion gradient, stimulated with noradrenaline | Pathological metabolic shift Fibrosis Defective calcium handling Impaired contractility | CO | ||
Chemical hypoxia induction (CoCl2 + glucose depletion) | Cardiac cell death Biomarker secretion Defective calcium handling Impaired contractility | CO | ||
Myocardial Ischemia | Gas-controlled hypoxia induction | Loss of cardiomyocyte viability Disruption of cellular ultrastructure Increased angiogenic potential Increased proinflammatory cytokine secretion | CO | |
Spatial oxygen gradients generated via continuous gas perfusion | Defective calcium handling Reduced contractile force Transcriptional changes Activation of inflammation | HoC | ||
Gas-controlled hypoxia induction | Impaired contractility Abnormal metabolic state Fibrosis Lactate normalization after reperfusion | |||
Heart Failure/ Cardiac Remodeling | Chronic catecholamine overstimulation | Impaired contractility Hypertrophy Cardiac cell death Increased NT-proBNP secretion | EHT | |
Tachycardia-induced cardiomyopathy | Chronic optical tachypacing | Faster contraction kinetics Shorter action potentials Shorter effective refractory periods | EHT | |
Diabetic cardiomyopathy | Chemical induction of diabetic conditions | Sarcomere disorganization Defective calcium handling Impaired contractility Hypertrophy Lipid accumulation Increased oxidative stress | 2D monolayer | |
Inflammatory cardiomyopathy (Myocarditis) | Proinflammatory stimulation (Cytokines or viral infection) | Impaired contractility Defective calcium handling Increased proinflammatory cytokine secretion | EHT |
