Table 1.
Nrf2/Keap1/ARE and diabetic complications.
| Diabetic complication | Pathogenesis | Nrf2- (or downstream-) mediated effects |
|---|---|---|
| Atherosclerosis | (i) oxLDL formation | (i) Protection from oxLDL transformation of phagocytic cells [77, 78] |
| (ii) Proinflammatory response in endothelial cells | (ii) Inhibition of proinflammatory response at atherosusceptible sites [71, 79] | |
|
| ||
| Heart failure | (i) Aberrant cardiac and ECM remodeling | (i) Blood pressure regulation [72] |
| (ii) Insulin resistance of myocytes | (ii) Protection of myocardium following ischemia | |
| (iii) Impaired regulation of intracellular calcium | (iii) Diminishes ROS and myocardial hypertrophy [99] | |
| (iv) Accumulation of AGE products | ||
|
| ||
| Diabetic nephropathy | (i) Renal oxidative and nitrosative stress | (i) Improvement of metabolic indices (e.g., polydipsia and polyuria) [110] |
| (ii) Mesangial cell proliferation, inflammation, fibrosis | (ii) Reversal in dysfunction of key growth factors and ECM proteins [111–113] | |
|
| ||
| Wound healing | (i) Keap1 overexpression | (i) Impairments in angiogenesis and reepithelialization [120] |
| (ii) Loss of wound redox homeostasis | ||
| (iii) Chronic inflammatory microenvironment | ||