Site-Specific Antioxidative Therapy for Prevention of Atherosclerosis and Cardiovascular Disease

Table 1

Inhibitors of ROS sources.

ROS sources	Inhibitors	Mechanisms
NADPH oxidase (Nox)	Calorie restriction exercise	(i) Reduction of visceral adipose tissue-derived inflammatory cytokines; (ii) Downregulation of AT1R
	ARBs	AT1R-induced activation of Nox
	Statins	Inhibition of ROCK
Xanthine oxidase (XO)	Calorie restriction exercise	(i) Inhibition of Nox-mediated EC damage; (ii) Inhibition of Nox-mediated EC damage
	ARBs	Inhibition of Nox-mediated EC damage
	Allopurinol oxypurinol	Direct inhibition of XO
	Calorie restriction exercise	Inhibition of oxidative stress and NOS uncoupling
Nitric oxide synthase (NOS)	ARBs; Statins; Allopurinol and oxypurinol	Inhibition of oxidative stress and NOS uncoupling
	BH4; Sepiapterin	Direct inhibition of NOS uncoupling
	Calorie restriction exercise	(i) Inhibition of electron leakage from ETC; (ii) Stimulation of mitochondrial biogenesis; (iii) Induction of UPs by activating PPARs
	Resveratrol	Stimulation of mitochondrial biogenesis
	TZD	Activation of PPAR-𝛾 and induction of UP2 and UP3
Mitochondrial electron; transfer chain (ETC)	WY-14643	Activation of PPAR-𝛼 and induction of UP2 and UP3
	Fibrates	Activation of PPARs and induction of UP2 and UP3
	ARBs	Activation of PPAR-𝛾 and induction of UP2 and UP3
	Statins	Activation of PPAR-𝛾 and induction of UP2 and UP3

AT1R: angiotensin II type 1 receptor, ARBs: angiotensin II type 1 receptor blockers, ROCK: Rho-kinase, ECs: endothelial cells, CMCs: cardiomyocytes, UP: uncoupling protein, PPAR: peroxisome proliferator-activated receptor, TZD: thiazolidinedione.