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Cardiovascular signaling group
Reactive oxygen and nitrogen species (ROS and RNS), and products formed via their reactions with cellular macromolecules such as lipids, play a significant role in the development of cardiovascular diseases, including atherosclerosis, restenosis, myocardial ischemia-reperfusion injury and heart failure. Cells have developed intricate mechanisms by which they respond to the overproduction of ROS and RNS, thereby increasing resistance against their deleterious effects. Such responses can be regulated by stress activated transcription factors (TFs), which can drive the transcription of cytoprotective genes in an integrated manner. The objective of our studies is to elucidate the mechanisms by which ROS, RNS and oxidized lipids elicit stress responses in the cardiovascular system, with a special emphasis on oxidative stress inducible transcription factor Nrf2. Moreover, the Nrf2-driven gene regulatory network and its interactions with other TFs are explored. Also, transgenic mice and mouse models of cardiovascular diseases will be utilized to examine the role of specific TFs and signaling pathways in pathophysiological processes.