Reactive oxygen species (ROS) act as secondary messengers and their moderate concentration is required in regulating a number of biological processes. An excessive generation of ROS induces oxidative stress and subsequent inflammation, both considered major drivers in the pathogenesis of renal and cardiovascular diseases. To counteract oxidative stress-induced damage, cells have also developed endogenous defense mechanisms. Nuclear factor erythroid 2-related factor 2 (NRF2) signaling has been a subject of interest. NRF2 is a basic leucine zipper transcription factor and is well recognized for its role in maintaining intracellular redox homeostasis by regulating the transcription of phase-II antioxidant enzymes in response to oxidative stress. Under basal conditions, NRF2 is regulated by Kelch-like ECH-associated protein 1 (Keap1), a repressor molecule that facilitates NRF2 proteasomal degradation. However, in response to stress, the conformation of the Keap1/NRF2 complex changes, resulting in the nuclear translocation of NRF2 protein, where it heterodimerizes with small musculoaponeurotic fibrosarcoma (sMAF) proteins. The complex further binds to the antioxidant response element (ARE) sequence to activate the transcription of ARE-dependent cytoprotective genes that confer protection against oxidative damage.
Targeted activation of NRF2 transcription factor has revealed its protective potential against various reno-cardiovascular abnormalities. Several ongoing clinical trials are investigating NRF2-based therapies for the treatment of kidney and cardiovascular diseases. Researchers have found that NRF2 is not only a key regulator of redox balance but also activates other cellular functions to improve overall health. Therefore, the identification of novel approaches targeting NRF2 signaling may lead to the implementation of clinical treatments that ultimately improve the care of patients with renal and cardiovascular diseases.
This Research Topic primarily welcomes submissions in the form of Original Research articles, Review articles and short communications from any groups investigating NRF2. Topics include, but are not limited to:
1. Homeostatic function of NRF2 signaling in renal and cardiovascular physiology
2. NRF2 mediated protection against kidney/cardiovascular diseases
3. Therapeutic strategies to induce NRF2 activation
4. Ongoing clinical trials targeting NRF2 in kidney/cardiovascular diseases
Reactive oxygen species (ROS) act as secondary messengers and their moderate concentration is required in regulating a number of biological processes. An excessive generation of ROS induces oxidative stress and subsequent inflammation, both considered major drivers in the pathogenesis of renal and cardiovascular diseases. To counteract oxidative stress-induced damage, cells have also developed endogenous defense mechanisms. Nuclear factor erythroid 2-related factor 2 (NRF2) signaling has been a subject of interest. NRF2 is a basic leucine zipper transcription factor and is well recognized for its role in maintaining intracellular redox homeostasis by regulating the transcription of phase-II antioxidant enzymes in response to oxidative stress. Under basal conditions, NRF2 is regulated by Kelch-like ECH-associated protein 1 (Keap1), a repressor molecule that facilitates NRF2 proteasomal degradation. However, in response to stress, the conformation of the Keap1/NRF2 complex changes, resulting in the nuclear translocation of NRF2 protein, where it heterodimerizes with small musculoaponeurotic fibrosarcoma (sMAF) proteins. The complex further binds to the antioxidant response element (ARE) sequence to activate the transcription of ARE-dependent cytoprotective genes that confer protection against oxidative damage.
Targeted activation of NRF2 transcription factor has revealed its protective potential against various reno-cardiovascular abnormalities. Several ongoing clinical trials are investigating NRF2-based therapies for the treatment of kidney and cardiovascular diseases. Researchers have found that NRF2 is not only a key regulator of redox balance but also activates other cellular functions to improve overall health. Therefore, the identification of novel approaches targeting NRF2 signaling may lead to the implementation of clinical treatments that ultimately improve the care of patients with renal and cardiovascular diseases.
This Research Topic primarily welcomes submissions in the form of Original Research articles, Review articles and short communications from any groups investigating NRF2. Topics include, but are not limited to:
1. Homeostatic function of NRF2 signaling in renal and cardiovascular physiology
2. NRF2 mediated protection against kidney/cardiovascular diseases
3. Therapeutic strategies to induce NRF2 activation
4. Ongoing clinical trials targeting NRF2 in kidney/cardiovascular diseases