A nitric oxide-dependent cross-talk between class i and III histone deacetylases accelerates skin repair

Abstract

Background: Nitric oxide (NO) regulates class I and IIa histone deacetylase (HDAC) function. NO production is regulated by class III HDACs (sirtuins). Results: NO functions as a bridging molecule between class I and sirtuins (SIRTs). Conclusion: The SIRT-NO-class I HDAC axis provides key signals during wound repair. Significance: Modulation of HDAC activity may play an important role in tissue regeneration. © 2013 by The American Society for Biochemistry and Molecular Biology, Inc.