For therapies based on human induced pluripotent stem cell (hiPSC)-derived 
cardiomyocytes (CM) to be effective, arrhythmias must be avoided. Towards 
achieving this goal, light-activated channelrhodopsin-2 (ChR2), a cation channel 
activated with 480 nm light, and a first generation halorhodopsin (NpHR1.0), an 
anion pump activated by 580 nm light, have been introduced into hiPSC. By using 
in vitro approaches, hiPSC-CM are able to be optogenetically activated and 
inhibited. ChR2 and NpHR1.0 are stably transduced into undifferentiated hiPSC 
via a lentiviral vector. Via directed differentiation, both wildtype hiPSC-CM 
(hiPSC(WT)-CM) and hiPSC(ChR2/NpHR)-CM are produced and subjected to both 
electrical and optical stimulation. Both hiPSC(WT)-CM and hiPSC(ChR2/NpHR)-CM 
respond to traditional electrical stimulation and produce similar contractility 
features but only hiPSC(ChR2/NpHR)-CM can be synchronized and inhibited by 
optical stimulation. Here it is shown that light sensitive proteins can enable 
in vitro optical control of hiPSC-CM. For future therapy, in vivo optical 
stimulation could allow precise and specific synchronization of implanted 
hiPSC-CM with patient cardiac rates and rhythms.