Molecular mechanisms by which iNOS uncoupling can induce cardiovascular dysfunction during sepsis: Role of posttranslational modifications (PTMs).

Abstract Human sepsis is the result of a multifaceted pathological process causing marked dysregulation of cardiovascular responses. A more sophisticated understanding of the pathogenesis of sepsis is certainly prerequisite. Evidence from studies provide further insight into the role of inducible nitric oxide synthase (iNOS) isoform. Results on inhibition of iNOS in sepsis models remain inconclusive. Concern has been devoted to improving our knowledge and understanding of the role of iNOS. The aim of this review is to define the role of iNOS in redox homeostasis disturbance, the detailed mechanisms linking iNOS and posttranslational modifications (PTMs) to cardiovascular dysfunctions, and their future implications in sepsis settings. Many questions related to the iNOS and PTMs still remain open, and much more work is needed on this.