Table 2.

Induced pluripotent stem cell models of cardiomyopathies in acquired metabolic syndromes

	Year (Ref)	Specific mutation	iPSC-CM in vitro phenotype	Cardiac muscle clinical phenotype
Type II Diabetes	2014 (32)	Two diabetic extreme phenotypes: Fast progression with CVD within 5 years Slow progression without CVD for 15 years Specific mutations not identified	iPSC-CMs exposed to diabetic milieu: Disorganized hypertrophy, intracellular lipid accumulation, altered calcium transients, cellular hypertrophy, oxidative stress Fast progression patient iPSC-CMs: Sarcomeric disarray, lipid-induced toxicity, reduced calcium transient frequency Slow progression patient iPSC-CMs: Less sarcomeric disarray, no lipid-induced toxicity or reduction in frequency of calcium transients	Systolic dysfunction and left ventricular hypertrophy, with subsequent risk of heart failure
Ischemia with ALDH2 deficiency	2014 (33)	Common heterozygous mutation in ALDH2 gene (ALDH2*2/1)	Increased oxidative stress, increased production of toxic aldehydes, decreased cell growth, decreased viability, increased cell apoptosis	Cardiac dysfunction and increased infarct size after myocardial infarction resulting from oxidative stress and nitroglycerin intolerance