The accumulation of DNA damage in human cardiomyocytes causes apoptosis which can lead to heart failure or other cardiovascular diseases. Although the effects of oxidative stress on heart health and on the DNA Damage Response network are well-known, the two fields have evolved as separate areas of research. The precise impact of oxidative DNA damage on cardiomyocyte contractile function still remains poorly understood. The human FANCJ helicase participates in multiple DNA repair pathways, including interstrand crosslink repair and double-stranded break repair. We have shown previously that FANCJ targets and unfolds 8-oxoguanine modified DNA secondary structures that arise from oxidative damage. We predict that human cardiomyocytes expressing mutations of FANCJ would be more susceptible to oxidative DNA damage and will negatively influence their contractile motion. To test this, hiPSC-CMs were treated with hydrogen peroxide, camptothecin, or bleomycin to induce different forms of DNA damage. The relative abundance of single-stranded DNA breaks and double-stranded DNA breaks were determined by modified comet assays, while contractile function was monitored using video-based detection methods. Cells that overexpress FANCJ protein were able to overcome the chemical stress from hydrogen peroxide. On the contrary, cells that produce a FANCJ K141/K142AA variant, which was previously characterized in the lab, resulted in a hypersensitivity to double-stranded DNA breaks. Based on this evidence, FANCJ plays a vital role in alleviating the effects of oxidative stress. Our long-term goal is to use the established methods to develop functional assays that characterize the cardiovascular risks of other FANCJ variants. These assays can be used to develop screening methods to identify patients who may be predisposed to FANCJ-associated cardiovascular diseases.