Protective Effects of Estrogen on Cardiovascular Disease Mediated by Oxidative Stress

Table 1

The mechanisms of estrogen inhibiting oxidative stress.

Mechanisms	The changes in oxidative stress	References
E2 decreased MAPK activity	The cardiomyocyte apoptosis and ROS production were reduced	[74, 77, 143, 180]
Estrogen decreased serum lipid peroxides	Overall antioxidant status was upregulated	[92, 150, 173, 181]
E2 inhibited NOX subunit p47phox	The reduction of superoxide anion production was inhibited	[155, 160]
E2 decreased NOX subunits gp91^phox, p22^phox, and p67^phox induced by Ang II	ROS production was reduced	[143, 158, 182, 183]
E2 upregulated the expression and activity of SOD induced by Ang II	ROS production wad reduced	[167, 184–190]
Estrogen restored antioxidant enzymes GPX1 and GPX4 expression levels	Oxidative stress balance was maintained	[158, 181, 189]
Estrogen increased the expression of the glutathione rate-limiting enzyme γ-glutamylcysteine synthetase	Oxidative stress balance was maintained	[168, 190, 191]
Estrogen maintained the bioavailability of NO by increasing the expression of eNOS mRNA and protein	The production of NO increased and oxidative stress was reduced	[84, 192–195]
ERα activated eNOS through the PI3/AKT signal pathway	The production of NO increased and oxidative stress was reduced	[175, 189, 195]
Estrogen increased the intracellular availability of the eNOS cofactor BH4 and prevented the uncoupling of eNOS	The production of eNOS-dependent ROS was reduced	[177, 178]