Richard T Premont

ArticleVolume 86, Issue 12p2325-2340.e9Open access Affiliations & Notes 1Institute for Transformative Molecular Medicine, Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA 2Department of Biochemistry, Case Western Reserve University School of Medicine, Cleveland, OH 44106, USA 3Harrington Discovery Institute, University Hospitals Cleveland Medical Center, Cleveland, OH 44106, USA 4Department of Population and Quantitative Health Sciences,...

Editor’s summary Hypertrophy of white adipose tissue due to triglyceride storage and steatosis in the liver due to excessive de novo lipogenesis have detrimental metabolic effects. Venetos et al. found that these processes were stimulated by the enzymatic removal of S-nitrosyl (SNO) groups from distinct protein targets in white adipose tissue and liver by the denitrosylase SCoR2.

Introduction NO is a ubiquitous redox signaling molecule with diverse roles in health and disease1. While early views highlighted the propensity for NO to signal via cGMP/protein kinase G 1 (i.e., indirectly via phosphorylation), this perspective overlooked NO’s redox function and has been superseded by direct enzyme-mediated signaling via the formation of S-nitrosothiols (SNOs; termed S-nitrsosylation)2.