Abstract
Cardiocerebral vascular disease (CCVD) is a common disease with high morbidity, disability, and mortality. Oxidative stress (OS) is closely related to the progression of CCVD. Abnormal redox regulation leads to OS and overproduction of reactive oxygen species (ROS), which can cause biomolecular and cellular damage. The Nrf2/antioxidant response element (ARE) signaling pathway is one of the most important defense systems against exogenous and endogenous OS injury, and Nrf2 is regarded as a vital pharmacological target. The complexity of the CCVD pathological process and the current difficulties in conducting clinical trials have hindered the development of therapeutic drugs. Furthermore, little is known about the role of the Nrf2/ARE signaling pathway in CCVD. Clarifying the role of the Nrf2/ARE signaling pathway in CCVD can provide new ideas for drug design. This review details the recent advancements in the regulation of the Nrf2/ARE system and its role and activators in common CCVD development.
Highlights
Cardiocerebral vascular disease (CCVD) is a common disease that seriously threatens human health, especially in people over 60 years old [1]
We focus on the Nrf2/antioxidant response element (ARE) antioxidant defense system and investigate its crucial role in various CCVD pathological processes
Many studies have reported the impact of the Nrf2 signaling pathway on the development of CCVD [13, 126]
Summary
Cardiocerebral vascular disease (CCVD) is a common disease that seriously threatens human health, especially in people over 60 years old [1]. When OS occurs, the Kelch-like ECH-associated protein 1 (Keap1)/Nrf signaling pathway is activated and regulates the expression of multiple antioxidants and detoxification enzymes to maintain intracellular homeostasis. The BTB-IVR domain binds to Cul and Roc to form a Keap1-Nrf2Cul3-Roc complex, which helps Nrf to undergo proteasomal degradation [19]. Nrf is a transcription factor containing 605 amino acids that were originally cloned from the human leukemia cell line K562 and belongs to the cap-n-collar (CNC) family of basic leucine zippers [23]. It is composed of seven highly conserved domains named Neh1-Neh, and each domain possesses a different function (Figure 1(b)). The Neh domain can suppress Nrf by interacting with retinoid X receptor [31]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
