Because pulmonary nitric oxide has been identified to play a critical role in pulmonary dysfunction in sepsis, we hypothesized that thoracic epidural anesthesia (TEA) modulates endothelial dysfunction via a nitric oxide-dependent pathway.
We hypothesized that TEA modulates pulmonary endothelial dysfunction in sepsis via an NO-dependent pathway.
Besides preventing microvascular thrombosis, enoxaparin may modulate inflammation and reduce endothelial dysfunction.
Through deacetylation of many transcriptional factors, SIRT1 modulates oxidative stress response, endothelial dysfunction, and inflammation, all key events acting in premature cellular senescence and aging [ 76] and also implicated in COPD onset and progression [ 77, 78].
Furthermore, erythrocyte antioxidant enzyme inactivation may modulate the putative effects of air pollutants on endothelial dysfunction.
Different reports have suggested that CoQ10 may improve endothelial dysfunction by "recoupling" eNOS and modulating NO-related signaling (Chew and Watts, 2004; Tsai et al., 2012).
We described in this review how oxidative stress, modulating p66Shc-NO pathway, impinges in many crucial aspects of diabetic endothelial dysfunction, representing a promising therapeutic objective.
Oxidative stress, which seems to play an important role in the development of endothelial dysfunction [ 23], is another parameter that was shown to be modulated by glucocorticoids [ 50].
Despite the significant progress in the understanding of endothelial dysfunction and vascular disease, no pharmacologically active agent has been developed to therapeutically modulate this connection.
ROS modulate multiple signal transduction pathways - activation of matrix metalloproteinase, vascular smooth muscle cell proliferation and death, endothelial dysfunction and lipid peroxidation - all of which are implicated in the process of atherogenesis [ 22].
