Cardiovascular diseases (CVDs) are the leading cause of death globally, with oxidative stress (OS) identified as a primary contributor to their onset and progression. Given the elevated incidence and mortality rates associated with CVDs, there is an imperative need to investigate novel therapeutic strategies. Nuclear factor erythroid 2-related factor 2 (Nrf2), ubiquitously expressed in the cardiovascular system, has emerged as a promising therapeutic target for CVDs due to its role in regulating OS and inflammation. This review aims to delve into the mechanisms and actions of the Nrf2 pathway, highlighting its potential in mitigating the pathogenesis of CVDs.
Keyphrases
- oxidative stress
- nuclear factor
- cardiovascular disease
- induced apoptosis
- signaling pathway
- toll like receptor
- diabetic rats
- ischemia reperfusion injury
- dna damage
- risk factors
- pi k akt
- type diabetes
- epithelial mesenchymal transition
- metabolic syndrome
- inflammatory response
- cell proliferation
- immune response
- heat shock protein
- drug delivery
- drug induced