Role of Endoplasmic Reticulum Stress in Atherosclerosis and Diabetic Macrovascular Complications

Table 1

Therapeutics targeting molecular components of ER stress and ER stress-induced apoptosis.

Drug	Mechanism	Potential indication	Reference
5-Aminoimidazole-4-carboxyamide-1-β-D-ribofuranoside (AICAR)	Reduction of ER stress by AMPK activation	Ischemic heart disease, heart failure, cardiac hypertrophy, atherosclerosis	[8–10]
BiP inducer X	Induction of GRP78	Heart failure, stroke	[11, 12]
Curcumin	Induction of GRP94	Heart failure, atherosclerosis, thrombosis, diabetes, diabetic cardiomyopathy, inflammation, dyslipidemia	[13]
CS-866	Reduction of ER stress by pressure-overload	Heart failure, cardiac hypertrophy	[14]
EN460	ERO1α inhibitor	Prevention/reduction of ER stress-induced oxidative stress	[15, 16]
Benzodiazepinones	ASK1 inhibitor	Atherosclerosis, cerebrovascular ischemia	[16]
QM295	ERO1α inhibitor	Prevention/reduction of ER stress-induced oxidative stress	[15]
Isoproterenol	Proteasome activation and assembly	Heart failure, atherosclerosis	[17]
Pioglitazone	Reduction of ER stress	Heart failure, atherosclerosis	[18]
Phenylbutyrate	Chemical chaperone	Heart failure, atherosclerosis, pulmonary hypertension	[19–21]
Pravastatin	Reduction of ER stress by pressure-overload	Heart failure, cardiac hypertrophy	[22]
Salubrinal	Prevention of eIF2a dephosphorylation	Heart failure, cardiac hypertrophy	[23]
SB203580	CHOP phosphorylation	Heart failure, cardiac hypertrophy, atherosclerosis	[24]
SP600125	Prevention of CHOP induction by stretch	Heart failure, cardiac hypertrophy, atherosclerosis	[24]
Sunitinib	IRE1 activation	Heart failure, atherosclerosis	[25]
Tauroursodeoxycholic acid (TUDCA)	Chemical chaperone	Heart failure, atherosclerosis	[19]