The zinc finger transcription factor Egr-1 plays an important role in cardiovascular biology. While binding complementary motifs on DNA in the target genes, Egr-1 either increases or decreases proteosynthesis of many proinflammatory and antiinflammatory mediators. In physiologic circumstances, these mediators support healing and regeneration of damaged tissue, mainly by conducting angioneogenesis. In pathologic circumstances these same mediators take an active part in promoting tissue injury. The participation of the transcription factor Egr-1 in the pathogenesis of atherosclerosis can be traced from the initial phases with the generation of foam cells as far as the onset of acute cardiovascular or cerebrovascular ischemic events. At the same time, transcription factor Egr-1 presents a would-be linker at the level of which converge many seemingly heterogenous atherogenic risk factors such as hyperlipidemic disorders, untoward rheologic changes of blood flow often encountered in arterial hypertension or various infectious agents, with Chlamydia pneumoniae belonging to the most deeply investigated ones. Protective effects of the known anti-atherogenic factors, such as the endogenous antiinflammatory cytokine interleukin-10 or the „pleiotropic“ effects of statins can be, at least in part, explained by their inhibitory influence on the activities of the transcription factor Egr-1.

        Key words: Egr-1, transcription factor, zinc fingers, DNA, genetic information, apoptosis, atherosclerosis. Ku.