Published: 01 February, 2022 | Volume 6 - Issue 1 | Pages: 001-018
Figure 2:
Courtesy ref no-15-Schemedetailing the starting of oxidative injury to the endothelium, the downstream consequences for endothelial impairment as well as the progresssion of oxidative stress. The layer of glycocalyx lining the apical surface of endothelial cells is significant for the sustenance of shear-stress and flow- modulated nitric oxide (NO) liberation and vasodilation of the endothelium. Sepsis- stimulated oxidative stress resulted in glycocalyx thinning and shedding, leads to the depletion of gap junctions, along with subsequently escalated permeability impairment as well as vascular leakage. Depletion s of gap junctions further greatly promotes extravasation of neutrophils in the circulation, modulated by β-integrins, via to the extracellular matrix. The resultant superoxide (O2−) that is generated can crosstalk with nitrosative species produced by inducible nitric oxide synthase (iNOS), generating the greatly reactive peroxynitrite (ONOO−) in addition to then hydrogen peroxide (H2O2) subsequently. Oxidative bursts from neutrophilsaid in escalating oxidative injury along with the downstream generation of pro-inflammatory cytokines which have the intrinsic capability of generating reactive oxygen species (ROS) along with reactive nitrogen species (RNS). Oxidative stress can further induce the recruitment of pro-coagulants to the site of injury, causing vascular congestion, ultimately impeding blood flow. Increased oxidative stress at the endothelium depletes besides resulting in oxidation of the pool of tetrahydrobiopterin (BH4), resulting in the uncoupling of endothelial nitric oxide synthase (eNOS) in endothelial cells, thereby enhancing the generation of ROS. Interleukin-1beta (IL-β); tumor necrosis factor-alpha (TNF-α), interferon-gamma (IFN-δ).
Read Full Article HTML DOI: 10.29328/journal.jcn.1001084 Cite this Article Read Full Article PDF
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