His recent research has focused on the role of the glucose-dependent, post-translational modifications of proteins by O-linked beta-N-acetylglucosamine moiety (O-GlcNAc) in mediating cardiomyocyte stress responses. Work from his laboratory has demonstrated that acute increases of O-GlcNAc levels are cardioprotective; conversely, in the setting of diabetes where O-GlcNAc levels are chronically elevated cardiomyocytes cell survival pathways such as autophagy are impaired in an O-GlcNAc dependent manner. Additional interests include the role of store-operated calcium entry (SOCE) in cardiomyocytes and how this is regulated by O-GlcNAc.