Involvement of lipoproteins, free radicals, and calcium in cardiovascular disease processes.

Low density lipoproteins have the capacity to alter cell calcium concentrations of a wide variety of cell types. The precise mechanism of physical interaction of the LDL or its products with the cell is not defined yet. There is more agreement about the calcium transport pathway affected. Most studies show an ability of LDL to alter transsarcolemmal calcium flux, probably through the slow calcium channel. However, internal stores of calcium like the sarcoplasmic reticulum also appear to be altered. These effects of LDL on cellular calcium homeostasis have potential importance in both physiological and disease settings. Oxidised LDL has even more potential significance than the native LDL in disease conditions. Free radical mediated oxidation of LDL during atherosclerotic and ischaemic conditions creates a molecule with even greater potency for altering cell calcium and ultimately cell function and viability. The interaction of this trio of compounds--LDL, free radicals, and cellular calcium--may be critical for the mechanism of pathogenesis in specific cardiovascular diseases. It will be important in the future to identify new therapeutic strategies to prevent their interaction.