Table 1.
Functional effects of the Nrf2/HO-1 signaling axis in cardiovascular diseases.
Cardiovascular disease | Effects | Reference |
---|---|---|
Viral myocarditis | Reduces inflammatory cytokine production and oxidative stress | [36] |
Reduces CVB3-induced myocarditis by activating GSK-3β | [37] | |
Rheumatic heart disease (RHD) | Inhibits signal transducer | [39] |
Cardiac tumors | Regulates antioxidant defense enzymes and counteracts oxidative stress | [40] |
Reduces toxicity with sulforaphane | [41] | |
Myocardial infarction (MI) | Involved the renin-angiotensin-aldosterone system | [42] |
Upgrades antioxidant genes | [43] | |
Myocardial ischemia reperfusion injury (MIRI) | Regulates the activation of thioredoxin-1 (Trx-1) through two antioxidant response elements | [45] |
Regulates ROS levels | [46] | |
Atherosclerosis (AS) | Strengthens antioxidative potential and alleviates inflammation | [47] |
Enhances the expression of HO-1 | [48] | |
Mediates atherosclerosis by saturated fatty acids | [49] | |
Arrhythmia | Produces antioxidant enzymes to reverse oxidative damage | [52] |
Activates the NO pathway | [53] | |
Hypertensive heart disease | Reverses the mitochondrial apoptosis effect | [54] |
Downregulates TGF-1/Smads in myocardial remodeling | [55] | |
Promotes lipolysis enzymatic activity | [56] |